A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright Ó2003 by ICON Group International, Inc. Copyright Ó2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Lung Cancer: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83712-0 1. Lung Cancer-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on lung cancer. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications.
Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON LUNG CANCER.......................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Lung Cancer.................................................................................. 5 E-Journals: PubMed Central ....................................................................................................... 65 The National Library of Medicine: PubMed ................................................................................ 70 CHAPTER 2. NUTRITION AND LUNG CANCER .............................................................................. 149 Overview.................................................................................................................................... 149 Finding Nutrition Studies on Lung Cancer .............................................................................. 149 Federal Resources on Nutrition ................................................................................................. 166 Additional Web Resources ......................................................................................................... 166 CHAPTER 3. ALTERNATIVE MEDICINE AND LUNG CANCER ....................................................... 171 Overview.................................................................................................................................... 171 National Center for Complementary and Alternative Medicine................................................ 171 Additional Web Resources ......................................................................................................... 206 General References ..................................................................................................................... 209 CHAPTER 4. DISSERTATIONS ON LUNG CANCER ......................................................................... 211 Overview.................................................................................................................................... 211 Dissertations on Lung Cancer ................................................................................................... 211 Keeping Current ........................................................................................................................ 213 CHAPTER 5. CLINICAL TRIALS AND LUNG CANCER .................................................................... 215 Overview.................................................................................................................................... 215 Recent Trials on Lung Cancer ................................................................................................... 215 Keeping Current on Clinical Trials ........................................................................................... 235 CHAPTER 6. PATENTS ON LUNG CANCER .................................................................................... 237 Overview.................................................................................................................................... 237 Patents on Lung Cancer ............................................................................................................ 237 Patent Applications on Lung Cancer......................................................................................... 260 Keeping Current ........................................................................................................................ 285 CHAPTER 7. BOOKS ON LUNG CANCER ........................................................................................ 287 Overview.................................................................................................................................... 287 Book Summaries: Federal Agencies............................................................................................ 287 Book Summaries: Online Booksellers......................................................................................... 288 The National Library of Medicine Book Index ........................................................................... 296 Chapters on Lung Cancer .......................................................................................................... 297 CHAPTER 8. MULTIMEDIA ON LUNG CANCER ............................................................................. 299 Overview.................................................................................................................................... 299 Video Recordings ....................................................................................................................... 299 Bibliography: Multimedia on Lung Cancer ............................................................................... 300 CHAPTER 9. PERIODICALS AND NEWS ON LUNG CANCER .......................................................... 303 Overview.................................................................................................................................... 303 News Services and Press Releases.............................................................................................. 303 Academic Periodicals covering Lung Cancer............................................................................. 307 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 309 Overview.................................................................................................................................... 309 U.S. Pharmacopeia..................................................................................................................... 309 Commercial Databases ............................................................................................................... 310 Researching Orphan Drugs ....................................................................................................... 311 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 315 Overview.................................................................................................................................... 315
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NIH Guidelines.......................................................................................................................... 315 NIH Databases........................................................................................................................... 317 Other Commercial Databases..................................................................................................... 319 The Genome Project and Lung Cancer ...................................................................................... 319 APPENDIX B. PATIENT RESOURCES ............................................................................................... 325 Overview.................................................................................................................................... 325 Patient Guideline Sources.......................................................................................................... 325 Finding Associations.................................................................................................................. 335 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 337 Overview.................................................................................................................................... 337 Preparation................................................................................................................................. 337 Finding a Local Medical Library................................................................................................ 337 Medical Libraries in the U.S. and Canada ................................................................................. 337 ONLINE GLOSSARIES ................................................................................................................ 343 Online Dictionary Directories ................................................................................................... 343 LUNG CANCER DICTIONARY................................................................................................. 345 INDEX .............................................................................................................................................. 429
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with lung cancer is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about lung cancer, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to lung cancer, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on lung cancer. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to lung cancer, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on lung cancer. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON LUNG CANCER Overview In this chapter, we will show you how to locate peer-reviewed references and studies on lung cancer.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and lung cancer, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “lung cancer” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: ·
Phytochemicals: The New Science of Eating Right Source: Fitness. p.108-110,112. April 1998. Summary: Kressy discusses phytochemicals, describing what they are and why some think they may help reduce the risk of heart disease, lung cancer, and other diseases, as well as assist in weight control. A chart lists the major phytochemicals and good sources for each. Several recipes are included.
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Emerging Concepts in Immunology, Clinical Practice, and Research for Dental Hygiene Source: Access. 15(8): 42, 45-49. September-October 2001.
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Contact: Available from American Dental Hygienists' Association. 444 North Michigan Avenue, Chicago, IL 60611. Summary: The Surgeon General's report on 'Oral Health in America,' released in 2000, described and evaluated the relationship of oral health to general health and well being, throughout the lifespan in the context of changes in society. This article reviews emerging concepts in immunology, clinical practice, and research, as they have an impact on dental hygiene and the provision of dental care. The author notes that oral health care is in the process of making the transition from a 'repair' model of care to a 'wellness' model of care. Evidence based care; emphasis on the skills of cognition, synthesis and communication; and client satisfaction are becoming more important in oral health care delivery. Other topics covered are gender-specific medicine, cancer, autoimmune diseases, diabetes, systemic lupus erythematosus (SLE), HIV, and AIDS, pharmaceuticals (drug therapy), tobacco and lung cancer, musculoskeletal health, current research at the National Institutes of Health (NIH), and the National Center for Complementary and Alternative Medicine (NCCAM, one of the Institutes of Health). 3 figures. 41 references. ·
Apolipoprotein E4: A Genetic Risk Factor for Late-Onset Alzheimer's Disease Source: Caring. 13(8): 24-28. August 1994. Summary: This article discusses the results of genetic research on Alzheimer's disease (AD) at Duke University. Researchers have found the first genetic risk factor for the type of AD that begins after age 60. The gene is a specific version of apolipoprotein E (ApoE), a protein that carries cholesterol through the bloodstream. These scientists assert that the inheritance of a specific form of ApoE raises the odds of having AD to a level comparable to that associated with smoking, getting lung cancer, or having high blood pressure that leads to a stroke. According to the authors, people with two ApoE4 alleles (one of three ApoE versions) are much more likely to develop AD than those who have none or only one copy. Once discovery of the effects of this protein on the brain and its involvement in the cause of late-onset AD occurs, researchers can design and test preventive therapies for AD.
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Vegetarian Diets: The Pluses and the Pitfalls Source: Rockville, MD: U.S. Department of Health and Human Services, Food and Drug Administration, Department of Agriculture, 4 p., 1994. Contact: Food and Drug Administration, Office of Consumer Affairs, 5600 Fishers Lane, HFE-50, Rockville, MD 20857. (301) 443-3170. Publication number (FDA) 93-2258. Summary: This article reviews the precautions that must be considered when adopting a vegetarian diet. The various reasons for choosing a vegetarian lifestyle include religious beliefs, expense, and personal beliefs. Vegetarians who abstain from dairy products or animal flesh face the greatest nutritional risks because some nutrients naturally occur mainly or almost exclusively in animal foods. These potential risks are explained. Next the health benefits of fruit and vegetable consumption are considered, including a lower risk of certain cancers, including prostate, breast, and colon cancer. Vegetarians are at lesser risk for obesity, atonic constipation, lung cancer, and alcoholism. Evidence is also good that risks for hypertension, coronary artery disease, diabetes, and gallstones are lower. It is generally agreed that to avoid intestinal discomfort, a person shouldn't switch to foods with large amounts of fiber all at once. The steps one should take for a gradual dietary change are considered. The article also includes a list of sources of nutrients of greatest concern for vegetarians who don't eat animal foods.
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Smoking and Chewing in Young People: The Power of Prevention is in Our Hands Source: Postgraduate Medicine. 101(3): 13-18. March 1997. Summary: This commentary serves as an introduction to a series of articles about lung cancer and smoking cessation. The author reflects on the use of tobacco by young people and the role of health care providers in preventing such use. The author begins with a discussion of the government's role in regulating the tobacco industry, particularly the sale and distribution of cigarettes and smokeless (spit) tobacco to young people. The article includes a sidebar of statistical information about tobacco use, primarily among young people. The author outlines specific step-by-step instructions for health care providers who wish to participate in preventing tobacco use in young people. 1 table. 7 references.
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National Cancer Institute's OCCAM Partners With NCCAM to Expand Research on Unconventional Cancer Source: Alternative Therapies in Health and Medicine. 5(4): 26-30. July 1999. Summary: This journal article discusses the recent establishment of the Office of Cancer Complementary and Alternative Medicine (OCCAM) within the National Cancer Institute (NCI), and its partnership with the National Center for Complementary and Alternative Medicine (NCCAM). Dr. J.D. White, director of the OCCAM, is the official liaison with other institutes and offices concerning alternative medicine research projects. Two cooperative NCI research projects involving complementary medicine had already been funded when the OCCAM was established. One is a phase III trial of the Gonzales protocol for pancreatic cancer, and the other is a phase II trial of shark cartilage for stages IIIA and IIIB lung cancer. To help advance additional high quality cancer research, Dr. White is working to develop the NCI's best case series, the process by which researchers submit their well-documented case reports for independent evaluation. The NCCAM's newly established Cancer Advisory Panel helps the OCCAM review the case studies of alternative cancer therapies, and makes recommendations about how to follow up on these evaluations. Areas of interest for future research projects include folk beliefs and practices and palliative care.
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Transbronchial Needle Aspiration Source: Gastroenterology Nursing. 14(2): 80-84. October 1991. Summary: Transbronchial needle aspiration biopsy is an endoscopic pulmonary procedure used to diagnose a variety of pulmonary conditions including staging patients with lung cancer and identifying nodules, masses, and benign disorders such as sarcoidosis. Transbronchial needle aspiration biopsy is a safe procedure, performed primarily with local anesthesia combined with intravenous sedation. This article is intended to educate nurses and technicians about the procedure of transbronchial needle aspiration and the instruments used. Four charts present the specifications for different types of biopsy needles. 1 figure. 4 tables. 8 references. (AA-M).
Federally Funded Research on Lung Cancer The U.S. Government supports a variety of research studies relating to lung cancer. These studies are tracked by the Office of Extramural Research at the National Institutes of
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Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to lung cancer. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore lung cancer. The following is typical of the type of information found when searching the CRISP database for lung cancer: ·
Project Title: A SIMULATION OF TOBACCO POLICY, SMOKING AND LUNG CANCER Principal Investigator & Institution: Levy, David T.; Professor; Pacific Institute for Res and Evaluation Calverton, Md 207053102 Timing: Fiscal Year 2002; Project Start 26-AUG-2002; Project End 31-JUL-2006 Summary: (provided by applicant) Because over 85% of lung cancer is caused by smoking, we focus on the effect of tobacco policies on lung cancer. We will extend a previously developed macro-simulation model, known as SimSmoke, to predict smoking-attributable lung cancer the effect of tobacco control policies on those deaths. The first major aim of this project is extending SimSrnoke to estimate and predict smoking-attributable lung cancer deaths. The model will be programmed to estimate the number of smoking-attributable lung cancer deaths to smoker and non smokers during the past ten years and predict deaths over the next 35 years, and to distinguish the number of deaths by age, gender and by racial/ethnic group, and distinguish the effects of quantity smoked and smoking prevalence. We will also distinguish the effect on lung cancer of factors other than smoking, other such as other risks and the effects of treatment. We also propose to determine the impact of tobacco control interventions on observed trends in mortality; and to determine if the interventions are having their expected population impact. Specifically, SimSmoke will be used to estimate the number of smoking-attributable deaths in the United States averted as a result of policies implemented in the last ten years, and estimate the number of smoking deaths that have been averted as a result of policies implemented in the last ten years in three states with proactive tobacco control policy. We will also consider the potential impact of policies in the future. In examining the effect of tobacco control policies, we will distinguish their effects on smoker and non-smoker deaths, their effects by age, gender, and racial/ethnic group, and their effects in terms of quantity reduction and smoking cessation. We will also add a new module to examine the effect of new tobacco products (low tar and cigarettes without certain additives) and non-tobacco products (inhalers) which may reduce lung cancer risk, and a module to consider how improved lung cancer detection and treatment may reduce smoking-attributable lung cancer deaths, and how they might be coordinated with tobacco control policies. A final goal of this project will be to critically examine the methods that are traditionally used to project lung cancer deaths, and determine how the estimates depend on the sensitivity to key parameters.
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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ALLOGENEIC TGF-B ANTISENSE CELL VACCINE FOR LUNG CANCER Principal Investigator & Institution: Fakhrai, Habib A.; Novarx Corporation 8395 Camino Santa Fe, Ste a San Diego, Ca 92121 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2003 Summary: (provided by applicant): The purpose of this study is to conduct a Phase II clinical trial in patients with incurable non-small cell lung cancer (NSCLC). Our aim is to induce antitumor immune responses by immunizing patients with an experimental vaccine comprised of four allogeneic NSCLC cell lines genetically modified with a TGFbeta 2 antisense vector. By blocking secretion of the immunosuppressive molecule TGF-beta in this manner we inhibit one of the major mechanisms by which tumor cells evade immune surveillance. Developing an effective therapy for the disease that accounts for 30 percent of all cancer-related deaths will benefit the approximately 180,000 new patients that develop lung cancer in the United States each year. In a previous clinical trial, we have shown that injections with gene-modified allogeneic tumor cells induced cellular immune responses to autologous tumor cells. In this trial, 18 patients will be randomized into three cohorts that will receive 1.25 x 10exp7, 2.5 x 10exp7, or 5 x 10exp7 TGF-beta antisensemodified vaccine cells. Following completion of this phase of the trial, an additional 48 patients will be enrolled in the two cohorts that demonstrate the best clinical responses. We anticipate that our treatment will induce measurable clinical responses in some of the treated patients. PROPOSED COMMERCIAL APPLICATIONS: The potential patient pool for this study is 180,000 patients annually in the United States. When considering other parts of the world, the potential patient pool is significantly larger. Once the Phase II clinical trial is completed, and the efficacy of our method is proved, we will perform the subsequent phases of our clinical trial phases, as well as the commercialization of our method in partnership with a pharmaceutical company that has the facility to mass produce and market our vaccine. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ALTERATIONS OF THE HUMAN SWI/SNF COMPLEX IN LUNG CANCER Principal Investigator & Institution: Reisman, David N.; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 24-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Candidate: The candidate is an Oncology fellow whose career goal is to become a translational researcher focusing on the molecular growth inhibitory pathways in lung cancer and the development of assays to detect neoplastic aberrance in these pathways both in vitro and in vivo. Research Plan: Lung cancer is the leading cause of cancer deaths in the United States. A reduction in the mortality will require the development of prognostic markers based on the understanding of growth inhibitory pathways. The SWI/SNF complex is a candidate to fill this critical need since it is likely required for function of the tumor suppressors, retinoblastoma (RB) and p130 (RB2). To understand how alterations in SWI/SNF may affect RB and p130 function, this proposal will determine the mechanisms for the downregulation of BRG and BRM (AIM 1), to clarify the role of BRG1 in RB mediated growth inhibition (AIM 2), to determine if BRG1 and BRM are lost or mutated in primary lung cancers (AIM 3), and to determine if BRG1 and BRM are important for p130 function
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(AIM 4). It is the goal of this training period to provide an intense research experience whereby expertise in molecular biology is gained leading to a career as a dually trained independent researcher. Environment: The excellent research environment at the Lineberger Comprehensive Cancer Center will promote the accomplishment of these specific aims. The candidate?s training and development will be directed by the dedicated mentorship and guidance of a senior and accomplished scientist, Dr. Bernard Weissman. Dr. Beverly Mitchell, who has many years? experience in mentoring successful physician/scientists, will provide protected research time and translational research guidance. Thus, this K08 funding period will allow the acquisition of new skills resulting in a series of publications leading to an independent cancer research career. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANALYSIS OF ETHNIC ADMIXTURE IN LUNG CANCER Principal Investigator & Institution: Barnholtz-Sloan, Jill S.; Internal Medicine; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 25-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): This proposal describes a five-year plan developed for a Cancer Prevention, Control, Behavioral and Population Sciences Career Development Award. It outlines a program that integrates education, teaching and research to develop my skills in statistical genetics, molecular biology, cancer biology, human genetics and genetic epidemiology. My research plan consists of two projects: (l) higher level genetic modeling of early onset lung cancer cases and controls with admixture versus ethnicity as a covariate and (2) application of an admixture, population substructure and disequilibria testing procedure to early onset lung cancer cases, population-based controls and nuclear families. Project l uses data from a funded study on early onset lung cancer of African-Americans and Caucasians. Nine candidate loci believed to be involved in lung cancer risk along with 35 population specific markers (PSAs) for Africans and Europeans combined, are being typed for each case and a matched population and familial control. An admixture algorithm will be written, programmed and tested on cases, controls and parents to estimate individual and population admixture, using the PSAs. Logistic regression models and decision tree models (classification and regression tree) will be compared when modeling the genotypes of the candidate loci and other collected environmental/descriptive variables, in order to assess the difference between using an ethnicity variable versus an individual admixture estimate variable. Project 2 will build on the already developed admixture estimation algorithm (Project l). I will develop a complete procedure that will estimate individual and population admixture and within population substructure and will test for induced linkage disequilibrium (LD) and Hardy-Weinberg disequilibrium (HWD), for all cases, controls and nuclear families. This procedure will be tested in a computer-based simulation, using the early onset lung cancer data as a model, in order to estimate the statistical power and test characteristics such as false-positive and falsenegative rates. Linkage disequilibrium mapping will also be performed on the study data. Both of these projects will address epidemiological study design issues about ethnicity and using population-based versus familial based controls. From the studies proposed, a recommendation could be made on how to utilize individual admixture information in the choice of controls for epidemiological studies. These projects will give me experience in developing methodology in statistical genetics and genetic epidemiology, while also helping me to better understand etiology of disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: AUTOANTIBODIES IN NSCLC AS MARKERS FOR DISEASE Principal Investigator & Institution: Hirschowitz, Edward A.; Medicine; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2003; Project Start 05-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): A variety of diagnostic and therapeutic strategies are being explored to change poor outcomes in lung cancer. Tumor markers, measured in peripheral blood, could complement the evolving clinical approach to lung cancer management. Autoantibodies to tumor-associated proteins may effectively expand the number and range of available serologic markers for lung cancer and be translated into a valuable test for lung cancer. Our preliminary data supports this hypothesis. We used phage-display and biopan techniques to identify multiple autoantibodies to known and unknown tumor-associated proteins in the serum of non-small cell lung cancer (NSCLC) patients. Using conventional immunochemical techniques and novel protein microarray we showed that autoantibodies to individual tumor-associated proteins are found in cancer patient sera and not in normals. Because no single antibody response is likely to be a comprehensive marker, we intend to build on these exciting data and develop an inclusive blood test for lung cancer by profiling sera for a variety of atuoantibodies. We have already identified 21 proteins recognized by autoantibodies in NSCLC patient sera and using these, plus additional proteins identified with these techniques; we will generate a comprehensive a panel of proteins used for antibody measurement. Fluorescent microarray technology, applied generally to gene discovery, is ideal for this purpose. Thus the primary goal of this proposal is to develop a novel blood test for NSCLC. To begin to expand the clinical relevance of this approach, a secondary goal is to show the association of autoantibody responses to tumor protein expression. The data shows feasibility and proof of concept that supports the rationale behind this proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BAYESIAN BIOMARKER MODELS FOR CANCER GENETICS STUDIES Principal Investigator & Institution: Thurston, Sarah W.; Biostatistics & Computational Biology; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 13-SEP-2002; Project End 31-JUL-2005 Summary: (Taken from the Investigator?s Abstract) This proposal aims to develop statistical methods which incorporate biomarkers and genetic information to improve estimates of cancer risk. This methodology will be developed using data from an ongoing study of lung cancer, smoking history, asbestos exposure, DNA adducts (a biomarker of smoking exposure), and genes associated with adduct formation and DNA repair (including CYP1A1 MSP1, GSTM1 and XRCC1). Currently the study has 2800 subjects, approximately half of whom are cases. Genotyping for multiple genes is ongoing. Phenol-related adducts have been measured in nontumorous lung tissue for 69 cases and in mononuclear blood cells for 38 cases and 42 controls. Polycyclic aromatic hydrocarbon adducts have been measured in normal lung tissue for 143 cases. The Bayesian paradigm, which can incorporate information from prior studies, will be used throughout. This paradigm can easily handle missing data such as lung adduct counts which cannot be measured in controls. All models for lung cancer risk will allow for synergistic effects between smoking and asbestos exposure. The specific aims of the proposal are: (1) to develop a model for DNA adduct counts given genes and smoking, and to then use the predicted adduct counts in a logistic regression model for lung
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cancer risk which corrects for the measurement error bias induced by using blood adducts instead of lung adducts in controls; (2) to develop a pharmacokinetic model for the number of blood adducts over time as a function of genes and changing smoking behavior, and to use the predicted cumulative adduct burden in a model for cancer risk; (3) by combining aims 1 and 2, to develop a model of cancer risk which both takes into account the changing adduct load over time and corrects for measurement error bias; (4) to extend the models in aims 1-3 to allow for nonlinear relationships between covariates and lung cancer risk using generalized additive models; (5) using new data, to compare the performance of the models developed in aims 1-4 to model which do not use biomarkers, and to assess the sensitivity of the outputs to both model and prior specification; and, (6) to develop guidelines on optimal sample sizes, sample selection and timing schemes for biomarker measurement, for future biomarker and exposuremediated cancer studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CANCER INTERVENTION AND SURVEILLANCE MODELING NETWORK Principal Investigator & Institution: Boer, Rob; Natural Scientist; Rand Corporation 1700 Main St Santa Monica, Ca 90401 Timing: Fiscal Year 2002; Project Start 25-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant) The proposed study is intended to develop a model for the comprehensive surveillance of population trends in lung cancer. This model will deliver estimates of the impact of cancer control interventions on: observed trends in incidence and/or mortality; the extent to which recommended interventions are having their expected population impact; the potential impact of new interventions on future national lung cancer trends; and the impact of targeted cancer control interventions on population outcome. The proposed model will be based on the Micro-simulation SCreening ANalysis (MISCAN) simulation model developed earlier for other cancer simulations and will be adapted to include an explicit model for the association between exposure to risk factors (smoking and diet) and risk for lung cancer as well as the time between exposure and effect. This risk-factor model will precede the comprehensive model for screening evaluation that includes the natural history of lung cancer, as well as exposure to screening and its health effects. This lung cancer screening evaluation model will be similar to MISCAN models that were previously successfully used for the evaluation of screening for breast, cervical, colorectal, and prostate cancer. As with other MISCAN models, the MISCAN-lung cancer model will simulate a full dynamic population, which makes it particularly suitable for surveillance of population trends. The model will be informed by the evidence from the literature, and it will be validated on several empirical longitudinal studies both on aspects concerning risk factors as well as screening. The proposed project will also develop a model for the evaluation of trends in survival from lung cancer that will optimally account for changes in reporting practice, in order to evaluate the impact of changes in therapy. This project provides a unique opportunity to integrate knowledge on all aspects of lung cancer that are relevant for the surveillance of population trends. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CAREER DEVELOPMENT PROGRAM Principal Investigator & Institution: Roth, Michael D.; Professor; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024
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Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-DEC-2005 Summary: (provided by applicant): The Career Development Program will utilize dedicated funds to prepare postdoctoral fellows or junior faculty for careers in translational lung cancer research. In addition, in well-justified selected cases, senior investigators who are already established in another area of research will be eligible in another area of research will be eligible for support to re-direct their research focus to lung cancer. The Career Development Selection Committee members represent a broad array of lung cancer-related disciplines including Medical Oncology, Surgical Oncology, Radiology, Thoracic Surgery, Radiation Oncology, Pathology, Pulmonary Medicine, Immunology, and Molecular Genetics. Committee members have extensive experience in mentoring trainees at all levels. Selection of Postdoctoral Fellows: Fellowship applications will be accepted from M.D. or Ph.D. post-doctoral trainees to work with a senior mentor. The fellow applicants will be required to submit a five-page research proposal and biosketch to the committee. The application will require a statement of career plans by the applicant as well as three letters of recommendation. One of these letters will be written by the primary mentor. The criteria for selection of fellows will be: 1) Quality of the scientific proposal, 2) The fellow's potential for an independent lung cancer research career, 3) Potential impact of the research on the field of lung cancer and, 4) Relevance to the overall translational research mission of the lung cancer SPORE program. Selection of junior faculty: The selection criteria noted above will also apply for the selection of junior faculty. In addition, the junior faculty applicant's department will be required to submit a letter of support delineating the commitment the commitment and support for the candidate. The process for selecting candidates for this program: An announcement will e made to all cancer center members two times per year. Distribution will also be directed to all graduate departments, training grant directors and clinical department chairs. The program will place special emphasis on recruitment of qualified women and minorities. The prospective mentor pool will be comprised of all of the senior SPORE investigators. In addition to the primary mentor, each postdoctoral or junior faculty trainee will be assigned an advisory committee. The advisory committee will consist of at least two additional mentors who will be meeting regulatory with the trainee to review work in progress. The overall purpose of this program will be to train well- qualified investigators in translational lung cancer research in a highly structured, academic setting. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CAREGIVER COPING SKILLS TRAINING FOR LUNG CANCER Principal Investigator & Institution: Keefe, Francis J.; Professor and Associate Director; Psychiatry; Duke University Durham, Nc 27706 Timing: Fiscal Year 2002; Project Start 06-JUN-2002; Project End 31-MAY-2007 Summary: (provided by investigator): Symptoms such as pain, fatigue, paroxysmal coughing, and dyspnea are major concerns of lung cancer patients and their caregivers. The focus in management of such symptoms traditionally has been on the patient. Studies of caregivers, however, have documented that the psychosocial impact of providing care to family members with lung cancer is profound. The ultimate goal of this research is to develop more effective ways to help patients and caregivers cope more effectively with problematic symptoms experienced by lung cancer patients. The proposed study seeks to evaluate the efficacy of a new, caregiver assisted coping skills training protocol. 500 early stage lung cancer patients (Stages I to IIIA) and their caregivers will be randomly assigned to one of two conditions: 1) Caregiver-assisted coping skills training-systematically trains caregivers in methods for guiding the patient
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in use of coping skills for symptom management (i.e. relaxation training, imagery, activity pacing, and communication skills), or 2) Cancer education and support-a comparison condition that provides patients and caregivers with information on the nature of lung cancer and treatment methods and controls for attention and contact. Assessment measures to be collected before and after treatment and at 4- and 14-months follow-up will include patient reports of major symptoms (pain, fatigue, coughing, and dyspnea), quality of life, depression, anxiety, self efficacy and quality of relationship with the caregiver and caregivers' ratings of mood, strain, and quality of relationship with the patient. If caregiver-assisted CST is effective, future studies could evaluate this training in other cancer populations (e.g. breast cancer, prostate cancer). Future studies could also identify the particular caregiver-assisted CST components (e.g. relaxation training, imagery training, or activity pacing methods) that contribute most to treatment effects. By isolating the active ingredients of training, one can streamline it, making it more cost-effective and more readily available to the larger population of patients having lung cancer. The proposed study rigorously evaluations methods for enhancing the effects of caregiver-assisted coping skills training in cancer patients and their caregivers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CHANGES IN DNA METHYLATION PATTERNS AS MARKER FOR CANCER Principal Investigator & Institution: Herman, James G.; Associate Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Lung cancer is the most common cause of cancer death in the United States, accounting for more life lost than breast, prostate, colon and rectal cancer combined. Of the estimated 190,000 individuals who are diagnosed each year, over 180,000 succumb to the disease. Increasing insight into the molecular basis of lung cancer pathogenesis offers hope to combat this disease. Lung cancer development and progression involves the inactivation of tumor suppressor genes and activation of oncogenes. While the accumulation of genetic alterations has been shown to be involved in the progression of lung epithelial cells from hyperplasia, metaplasia, dysplasia, carcinoma in situ, invasive carcinoma, and finally metastatic carcinoma, recent work in the previous funding period of this SPORE project has demonstrated that epigenetic changes represent another important molecular change in lung cancer. With that background, the specific aims of the current proposal are: Specific aim 1. To utilize a newly derived microarray approach to identify novel hypermethylated genes which will help comprise methylation marker panels providing for full coverage of the non-small cell lung cancer genome. Specific aim 2. To utilize the marker panels from specific aim 1 to develop an epigenetic progression model based upon studies of precursor lesions and early stage lung cancer. Specific aim 3. To test the epigenetic marker panels for their efficacy as prognostic markers to identify patients with Stage I non-small cell lung cancer at very high risk for rapid disease recurrence. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHEMOPREVENTION OF TOBACCO RELATED CANCER IN ANIMALS Principal Investigator & Institution: Pereira, Michael A.; Director; Pathology; Medical College of Ohio at Toledo Research & Grants Admin. Toledo, Oh 436145804
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Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2005 Summary: (provided by applicant): Our overall goal is to develop biomarkers for chemoprevention studies of cigarette smoke-related cancers that can be translated to clinical studies in former smokers. To obtain this aim, we propose: Specific Aim 1: Develop biomarkers for chemoprevention of lung cancer in former smokers using a mouse model for lung cancer and related biological and molecular alterations; and Specific Aim 2: Develop biomarkers for chemoprevention of bladder cancer in exsmokers using a rat model for urinary bladder cancer and associated biological and molecular alterations. Our hypothesis is that chemopreventive agents will decrease cancer incidence by modulating and reversing biological and molecular alterations in phenotypically normal tissue, precancerous tissues and tumors. Further, we hypothesize that the modulation of the biological and molecular alterations can be developed as biomarkers for chemoprevention in animal and clinical studies including studies in former smokers. To accomplish Aim 1, lung tumors will be induced in strain A mice by exposure to cigarette smoke, benzo(a)pyrene and 4-(Methyl nitrosamino)-1-(3- pyridyl)1-butanone (NNK) and to accomplish Aim 2, bladder tumors will be induced in F344 rats by N-butyl-N-hydroxybutyl)nitrosamine (OH-BBN). After exposure to the carcinogens including cigarette smoke has ceased the animals will be administered the chemo-preventive agents: budesonide and the farnesyl transferase inhibitor, R115777 in the lung studies and budesonide, ketoprofen and sulindac in the bladder study. Biological and molecular alterations of cell proliferation, apoptosis, methylation of genes (both hypomethylation of protooncogenes and hypermethylation of tumor suppressor genes) and alteration in mRNA and protein expression will be determined in phenotypically normal tissues, precancerous lesions and tumors at different times during the progression to cancer. The ability of the chemopreventive agents to modulate and reverse these biological and molecular alterations in tissue and lesions will be determined in parallel with the ability of the agents to prevent cancer. Thus, biological and molecular alterations that are modulated in parallel with the prevention of cancer by the chemopreventive agents will be indicated as biomarkers for chemoprevention studies including those in former smokers where the agents will similarly be administered after exposure to cigarette smoke had ceased. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: COMPUTER AIDED DIAGNOSIS OF LUNG CANCER Principal Investigator & Institution: Chan, Heang-Ping; Professor; Radiology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2006 Summary: (provided by applicant): Lung cancer is the leading cause of cancer deaths in both men and women. A 70 percent five-year survival rate has been reported when the lung cancer is diagnosed at a local stage, compared to 2 percent when distant metastases are found. Recent studies indicate that helical CT may be an effective screening tool for lung cancer. The American College of Radiology Imaging Network (ACRIN) will begin a randomized controlled trial of helical CT for lung cancer screening to evaluate its efficacy. Analysis of CT images to detect lung nodules is a demanding task for radiologists. Some lung nodules will likely be overlooked because of the overwhelming amount of information to be interpreted. Characterization of detected nodules to reduce unnecessary biopsies will also become more important as the number of thoracic CT exams increases. Computer-aided diagnosis (CAD) can be a viable approach to improving the accuracy and efficiency of lung cancer detection in CT images. It will be particularly useful if lung cancer screening with CT is implemented. The goal of the
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proposed project is to develop a CAD system for early detection of lung cancers on thoracic helical CT images. We hypothesize that an accurate CAD system (1) can be developed, (2) can be used as a second opinion to assist radiologists in interpretation of thoracic CT exams, and (3) will improve radiologists' accuracy for lung cancer detection. We will develop advanced computer vision techniques to automatically segment helical CT images, detect candidate pulmonary nodules, differentiate nodule and normal pulmonary structures, and estimate the likelihood of malignancy of the nodules. Computerized image segmentation and feature extraction techniques will be developed based on expert knowledge and image characteristics. Statistical classifiers, fuzzy classifiers, and artificial neural networks will be designed to differentiate nodules and normal structures, as well as to characterize malignant and benign nodules. Quantitative CT phantom studies will be performed to develop reliable methods for estimating the calcium concentration of nodules and estimating nodule volume on CT images so that these features can be used in our CAD system for malignancy detection. Observer performance studies using receiver operating characteristic (ROC) methodology will be conducted to evaluate the effects of CAD on radiologists' detection and classification of lung nodules in CT images. A large public database of helical CT cases to be collected by an NIH-supported consortium will be the main data source for the development of the computer vision techniques. The innovations of this project include: (1) developing region-specific computer vision method for detection of lung nodules; (2) eliminating the vascular tree in the helium for false positive reduction, (3) exploring interval change analysis for classification of malignant and benign nodules; (4) developing a quantitative method for measuring the calcium concentration of nodules for improved characterization of calcified nodules, and (5) performing ROC studies to evaluate CAD's ability to assist radiologists in the detection and characterization of lung nodules in CT studies. It is expected that the proposed studies will result in an effective CAD system for lung cancer diagnosis. When fully developed and clinically implemented, a CAD system for lung nodules will increase the efficacy of lung cancer screening with helical CT, improve early detection, and improve the chance of survival of patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: COMPUTER-AIDED DIAGNOSIS TO ENHANCE THORACIC CT IMAGE Principal Investigator & Institution: Lure, Yuan-Ming F.; Caelum Research Corporation 1700 Research Blvd, Ste 100 Rockville, Md 208506121 Timing: Fiscal Year 2003; Project Start 01-MAY-2001; Project End 31-MAY-2005 Summary: (provided by applicant): In the US alone, it is estimated that lung cancer caused a total of 161,900 deaths in 2000. The 5-year survival rate in the US is 13% when all stages are considered. Substantial evidence suggests that early detection of lung cancer may reduce mortality for patients with stage T1 NxMx. High-resolution CT can detect lung nodules when they are still small. But it is currently difficult for radiologists to distinguish those that are malignant from those that are benign. We propose to develop a computer-aided diagnosis (CAD) system to assist radiologists in the diagnosis of lung cancer in thoracic computed tomography (CT). The CT-CAD system will enable radiologists to robustly measure and analyze the suspicious lesions, effectively visualize the region of interest, and improve differentiation between malignant and benign nodules. Specifically, this SBIR phase II effort includes (1) continuous development of dedicated lung cancer diagnostic tools, (2) development of a complete CT-CAD system for accurate analysis of small lung lesions, (3) evaluation of the proposed system functions and integration of them in a CAD-specific 3D visualization platform; and (4)
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evaluation of the radiologists performance with and without using the CT-CAD system using the MRMC-ROC study protocol. The successful development of the proposed CTCAD system can significantly benefit the existing CT lung cancer diagnosis in two-fold: (a) improving sensitivity for lung cancer detection and (b) improving the accuracy of lung cancer diagnosis in CT and leading to reduction of unnecessary biopsies. We expect that this CT-CAD can facilitate remote reading by experts and will also increase radiologists' efficiency in reading large image arrays and reducing the observer variations in thoracic CT image interpretation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CORE--CLINICAL RESEARCH Principal Investigator & Institution: Sandler, Alan; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): The role of the Clinical Trials Core is to provide expertise in the development, implementation and coordination of all translational clinical trials resultant from the other SPORE projects that will ultimately lead to a better understanding of the biology of lung cancer. This improved understanding will ultimately lead to improvements in the treatment of lung cancer. To achieve this goal, the major responsibilities of the Clinical Trials Core will be 1) Provide expertise in the development and implementation of translational clinical trials related to the other SPORE projects 2) Accrual of patients to participate in SPORE initiated trials, 3) Timely and accurate collection of data, and 4) Accessibility of data for analysis by the various SPORE researchers at Vanderbilt university as well as researchers at other Lung SPORE sites. During the first year there will be at least seven translational trials open for accrual. These trials will serve to further the scientific knowledge regarding the role of 1) molecular fingerprinting and outcome analysis in resectable patients with lung cancer and 2) angiogenesis in lung cancer. More specifically, the impact of matrix metalloproteinases and their inhibition; the role of VEGF and its inhibition; the role of COX-2 and its inhibition on the outcomes of patients with lung cancer treated with either surgery, radiation, chemotherapy and/or their combination in patients with lung cancer. Over the five year course of the SPORE grant, trials will open and close. One of the goals of this SPORE is that the successful completion of these early pilot trials will ultimately lead on to larger scale, multi-institution trials for confirmation of our results. A second goal is that additional translational clinical trials will be designed based upon the results of the early pilot trials as well as the ongoing research of the participating SPORE investigators. The current pilot trials will thus serve as the template for further translational research in lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--TISSUE FACILITY Principal Investigator & Institution: Johnson, Joyce; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): The tissue resource and pathology core will provide high-quality tissue specimens and basic histology and pathology services in support of lung cancer research performed within the SPORE. The specimens, information, and services provided by the core will be carefully quality-controlled, and informed consent and patient confidentiality will be consistently maintained. The primary function of the
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core will be to procure, archive, and distribute to SPORE investigators lung cancer tissue specimens and paired normal tissue which has been characterized histopathologically, along with relevant clinical data, if allowed by the specific protocol involved. Such tissue will be maintained in a variety of conditions to allow DNA, RNA, or protein studies, depending on the research requirements of individual investigators. The core will also provide laser capture micro-dissection technology. Data obtained from individual specimens will be maintained in the core's database. Establishment of the core functions will be facilitated by the prior existence of the Vanderbilt-Ingram Cancer Center's Human Tissue Acquisition and Pathology Shared Resource, established in 1993 and managed since its inception by Roy Jensen, MD, who is a co-Principal Investigator on this core. The specific aims of this core are: 1. To collect, accession, and store tissues removed from lung cancer patients and normal "control" lung as outlined in the appropriate research informed consent, and to preserve these tissues frozen, formalin-fixed and embedded, and on touch imprints, in order to support lung cancer SPORE projects. 2. To maintain a centralized, computerized database of all specimens with basic demographic and pathologic information to permit the integration of findings by SPORE investigator through molecular assays and other laboratory studies with risk factor data and follow-up. 3. To maintain the confidentiality and integrity of the database, through keyed numeric identifier assigned by the tissue core for each specimen. 4. To provide high quality control of all well-characterized tissues in both human and murine with respect to preservation and histopathologic characterization. 5. To provide micro-dissected lung tumor and matched control cell populations from paraffin and frozen section for appropriate projects (e.g. project 2). 6. To provide immunohistochemical evaluation and quantitation in both human lung and murine tissues. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CREATION AND CHARACTERIZATION OF MOUSE MODELS OF HUMAN L Principal Investigator & Institution: Jacks, Tyler E.; Associate Investigator; Center for Cancer Research; Massachusetts Institute of Technology Cambridge, Ma 02139 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-MAR-2004 Summary: Lung cancer is the third most common cancer in the United States and is the leading cause of cancer related mortality for both men and women, with 171,500 new cases and 165,600 deaths projected for 1998 in this country. Although smoking cessation trends among adults may result in fewer lung cancer cases in the short to intermediate term, smoking rates among young adults seem to be on the rise. In addition, smoking rates in other parts of the world guarantee that lung cancer will remain a major public health problem worldwide for years to come. One reason for the poor rate of survival of individuals diagnosed with lung cancer is the frequently advanced stage of the disease upon presentation. Thus, there is a clear need to characterize markers associated with early-stage lung cancer to improve methods of diagnosis. Novel therapies for the treatment and prevention of the disease are also wanting. The mouse has been used to model human lung cancer extensively over the past several years in a variety of circumstances, including in spontaneous tumor models, chemically-induced models using a variety of agents, and in certain transgenic strains. Although these studies have confirmed that the mouse can be an adequate model of the early stages of human nonsmall cell lung cancer (NSCLC) (the predominant form of human lung cancer), the methods used in the derivation of these models (e.g., treatment with chemical carcinogens or transgenic expression of viral oncoproteins) and their limited stage of
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progression has lessened enthusiasm somewhat. This MMHCC team proposes to create novel mouse models of human NSCLC and to characterize these strains in a variety of ways directed toward their proper validation. The strains will harbor targeted activating mutations in the K-ras oncogene (frequently mutated in human NSCLC) and constitutive or conditional loss-of-function mutations in the lung tumor suppressor genes p53 and the Ink4A locus. Existing and future mouse models of NSCLC will be examined by histological analysis in consultation with a veterinary and human clinical pathologist. Mouse tumors will be subjected to extensive DNA and RNA analysis, in part with reference to known molecular changes in human NSCLC and in part in an effort to identify changes that can then be screened for in human tumor samples. The mouse models of NSCLC will be used in cigarette smoke exposure studies and will be used to evaluate investigative chemotherapeutic and chemopreventative agents. A genetic modifier screen will be performed as part of the characterization of one of these strains. Finally, these mouse lung cancer models will be used in the development of novel non-invasive imaging protocols for primary lung tumors and metastatic lesions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DEFINING THE SENSITIVITY & SPECIFICITY OF BIOMARKERS Principal Investigator & Institution: Belinsky, Steven A.; Director Lung Cancer Program; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Lung cancer is the most common cause of cancer death in the United States, accounting for more life lost than breast, prostate, colon and rectal cancer combined. Of the estimated 190,000 individuals who are diagnosed each year, over 180,000 succumb to the disease. Increasing insight into the molecular basis of lung cancer pathogenesis offers hope to combat this disease. Lung cancer development and progression involves the inactivation of tumor suppressor genes and activation of oncogenes. While the accumulation of genetic alterations has been shown to be involved in the progression of lung epithelial cells from hyperplasia, metaplasia, dysplasia, carcinoma in situ, invasive carcinoma, and finally metastatic carcinoma, recent work in the previous funding period of this SPORE project has demonstrated that epigenetic changes represent another important molecular change in lung cancer. With that background, the specific aims of the current proposal are: Specific aim 1. To utilize a newly derived microarray approach to identify novel hypermethylated genes which will help comprise methylation marker panels providing for full coverage of the non-small cell lung cancer genome. Specific aim 2. To utilize the marker panels from specific aim 1 to develop an epigenetic progression model based upon studies of precursor lesions and early stage lung cancer. Specific aim 3. To test the epigenetic marker panels for their efficacy as prognostic markers to identify patients with Stage I non-small cell lung cancer at very high risk for rapid disease recurrence. case-control study comparing sputum samples from 33 incident cases and their matched controls was conducted. The presence of any of four methylation markers examined was associated with a 6.3-fold increase in the risk for lung cancer. Moderate atypia or worse in sputum was also associated with a 4.1-fold increase in the relative risk for lung cancer over this time period. Interestingly, the methylation markers and cytology were not highly correlated with each other, though each was predictive of lung cancer risk, hence the two biomarkers were synergistic in conveying a 13.8-fold increase in relative risk. Through this cohort and a Phase II chemoprevention trial, studies with appropriate power will be designed to test specific hypotheses related to prediction of cancer risk and monitoring of chemoprevention interventions. This project is an inter-SPORE collaboration with
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Colorado that links clinical and epidemiologic findings with the development of promoter hypermethylation as molecular markers through the following three specific aims. Specific aim 1 will conduct a nested, case-control study within the Colorado cohort to evaluate longitudinally the ability to detect in sputum genes inactivated by methylation as biomarkers for predicting lung cancer risk either alone or in combination. Specific aim 2 will examine the dynamics of the field cancerization process by determining the concordance between methylation changes detected in sputum and bronchial biopsies from the same subject. Specific aim 3 will determine whether a panel of methylation markers can be used to predict the efficacy of the chemopreventive agent Iloprost in a randomized Phase II study through evaluation of bronchial biopsies and sputum collected at study entry and following completion of the intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DEVELOPMENTAL RESEARCH PROGRAM Principal Investigator & Institution: Strieter, Robert M.; Professor and Chief; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-DEC-2005 Summary: (provided by applicant): The UCLA Lung Cancer Spore Developmental Program will be used as a source of seed funding with two primary goals: 1) to encourage and explore innovative translational research ideas which focus on lung cancer research, and 2) to encourage successful researchers working in other fields to focus their expertise toward the development of innovative translational projects in lung cancer research, and 2) to encourage successful researchers working in other fields to focus their expertise toward the development of innovative ideas for funding will occur through a peer review mechanism. Announcements for developing funding opportunities will be made two times each year, using a highly successful organizational structure offered by the UCLA Jonsson Comprehensive Cancer Center. The request for applications will be posted by e-mail, regular mail and distribution of flyers of flyers to the more than 300 members of the Cancer Center. The Developmental Programs Committee will then meet to select the most meritorious Lung Cancer Research applications. The criteria for judging these applications will be: 1) scientific merit, 2) translational potential, 3) relevance to lung cancer, 4) potential for collaborative research and, 5) qualifications of the investigative team to perform the Committee, the Executive Committee will determine the factual funding line. The Internal and External Advisory Boards will review these funding decisions biannually. Applicants will be funded for a maximum of two years. Funding for the second year will be contingent on documented progress made during the first year of funding. Annual progress reports documenting research progress, publications and submission for additional outside funding will be required. Only those projects that demonstrate a productivity and clear translational potential will be funded for a second year. In addition, all Developmental Research Program funded investigators will be expected to present at least two times each year at the SPORE Review of Work in Progress meetings. This will provide the Executive Committee the opportunity to assess the progress of the investigators to be knowledgeable about on- going research. At the conclusion for additional NIH or other funding, or their project will be incorporated as a larger project within the SPORE. The Executive Committee will make the ultimate decisions regarding starting and stopping funding for individual projects after receiving input from the Developmental Programs Selection Committee. These decisions will be reviewed and critiqued by the Internal and External Advisory Boards. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DIET AND GENETIC RISKS FOR LUNG CANCER Principal Investigator & Institution: Patterson, Ruth E.; Associate Member; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2001; Project Start 05-MAR-2001; Project End 31-DEC-2002 Summary: (Applicant's Description) This proposal is for an investigation into the associations of diet, and interactions of diet and genetic polymorphisms, with the risk of lung cancer. Data are from 18,314 men and women enrolled in a chemoprevention trial of beta-carotene and retinol (CARET). After a mean of 7.4 years of follow up, CARET has endpoint data on almost 800 cases of lung cancer. Dietary intake was measured with a food frequency questionnaire. Serum micronutrient and genetic polymorphisms have been analyzed for 388 lung cancer cases and 753 controls. Our specific aims are: 1. To better understand the association of fruit and vegetable intake with the reduced risk of lung cancer. Fruit and vegetable intake will be measured as: (i) servings per day (total and grouped by phytochemical content), (ii) micronutrient associated with fruits and vegetables, including vitamins C and E, folate, and carotenoids, and (iii) serum carotenoids and vitamin E. 2. To examine whether the associations of fruit and vegetable intake with lung cancer risk are modified by genotypes of carcinogen metabolizing enzymes (i.e., CYP2D6, CYP2El, CYP1Al, GSTM1, GSTT1, and EH). We will conduct cohort analyses for dietary intake data and case control analyses for laboratory based studies. Although the baseline dietary data have been collected and the laboratory analyses (for serum micronutrients and genotypes) have been completed, there are no CARET investigators with expertise in nutrition science who are funded to conduct these analyses and write the associated manuscripts. Therefore, to meet the specific aims proposed above, we request support for nutritional epidemiologists, a statistician, molecular biologist, and the staff support needed to publish the findings. This work addresses important questions about the etiology and prevention of lung cancer, and can be completed with a modest amount of funding in addition to what has already been invested in this large chemoprevention trial. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DNA CARCINOGENESIS
DOUBLE
STRAND
BREAK
REPAIR
IN
TOBACCO
Principal Investigator & Institution: Bedford, Joel S.; Professor; Environmental & Radiological Health Sciences; Colorado State University Fort Collins, Co 80523 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant): Despite strong epidemiological data associating tobacco smoke to lung cancer, the mechanism of carcinogenesis by tobacco chemicals is not well understood. Among those exposed to tobacco smoke, only a certain portion develop lung cancer suggesting the involvement of genetic factor(s) in the susceptible population. A difference in DNA repair ability has been suggested for the explanation of the susceptibility. Of the various DNA repair pathways, a relationship between nucleotide excision repair and tobacco carcinogens (e.g. benzo[a]pyrene) has been well documented. However, DNA double strand break (DSB) repair, another important repair pathway, has rarely been studied with tobacco chemicals in mammalian systems. Since a recent study revealed a positive association between lung cancer and the reduced activity of a protein involved in DNA DSB repair, this application is initiated to confirm and extend the study on the role of DNA DSB repair in tobacco carcinogenesis. DNA DSB is the most destructive form of DNA damage and can lead to cell death, mutation and transformation if not repaired or mis-repaired. An efficient way to study
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the role of DNA DSB repair is to use DNA DSB repair deficient mutant cell lines exposed to tobacco chemicals. Specific Aim 1 addresses: Various rodent and human DNA DSB repair deficient cell lines will be treated with several tobacco carcinogens and cigarette smoke condensate (CSC), and comparisons will be made to wild type cells with regard to cell survival and mutation frequency. This is to test the hypothesis "Mammalian cells utilize DNA DSB repair mechanism or protein(s) associated with DNA DSB repair in the recovery process of DNA damage induced by tobacco carcinogens". Further molecular studies are suggested based on the cell line studies. These studies have the potential to identify a new tobacco sensitive sub-population. The experiments in Specific Aim 2 are proposed based on our recent finding that lung cancer sensitive BALB/c mice showed a mild DNA DSB repair defect. Specific Aim 2 puts forward the studies on the cell viability, DNA DSB formation and chromosome rearrangements in alveolar macrophage (AM), lymphocytes and lung epithelial cells from BALB/c and C57BL/6 (control) mice exposed to tobacco carcinogens. Two hypotheses will be tested in this aim: (1) Cells from BALB/c mice show a higher level of chromosome misrejoining which is detected by a sensitive premature chromosome condensation (PCC) assay in interphase chromosomes combined with/without fluorescence in situ hybridization (FISH)." (2) There is a good correlation between the sensitivity data with lymphocytes and those with AM and/or lung epithelial cells. The proposed experiments not only provide new mechanistic insight on the initial step for tobacco carcinogenesis, but also help furnish sensitive diagnostic tools to identify lung cancer susceptible individuals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: EPIDEMIOLOGIC STUDIES OF LUNG CANCER RISKS IN NSAID USERS Principal Investigator & Institution: Zheng, Wei; Professor; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): Cumulative evidence from in vitro and animal studies suggests that the enzyme cyclooxygenase-2 (COX-2) is important in the development and progression of lung cancer. Epidemiologic studies evaluating the association between the use of aspirin (an inhibitor of COX-2) and the risk of lung cancer have been conflicting, and no study has been conducted to evaluate non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs). Using pre-recorded drug prescription databases of the Tennessee Medicaid program and North Jutland County of Denmark, we propose to conduct two studies in these populations to examine the effect of NSAID use on the risk of lung cancer. The first is a retrospective cohort study of over 10,000 enrollees of the Tennessee Medicaid Program who were diagnosed with chronic obstructive pulmonary diseases (COPD) during the period of 1980 to 2002. The second is a population-based, retrospective cohort study of over 150,000 users of NSAIDs in the general population of North Jutland County during the period of 1991 to 2002. Within the Danish cohort will be a nested case-control study of 350 cases and 700 controls, in which relevant information will be obtained on over the counter (OTC) analgesic use, as well as cigarette smoking and other potential confounding factors. The two studies proposed here complement each other and provide for an international comparison of NSAIDs as possible lung cancer chemoprevention agents. Because the data on NSAID use have already been collected, the studies will be very cost-efficient. More importantly, the use of pre-recorded pharmacy records minimizes potential errors in exposure assessment and provides a major advantage over existing cohort studies in
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evaluating the potential chemopreventive effect of NSAIDs. Given the high incidence and mortality of lung cancer and high prevalence of NSAID use, the results from our studies may have important public health implications in lung cancer prevention, and could set the stage for future randomized trials of COX-2 inhibitors in cancer prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ETHNIC DISPARITIES, QUALITY OF LIFE AND MODE OF DEATH Principal Investigator & Institution: Fouad, Mona N.; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 28-SEP-2001; Project End 31-AUG-2006 Summary: Description This 3-year special project proposes to examine racial/ethnic variations in and associations between disease-specific symptoms, quality of life (QOL), and site of death during the terminal stages of lung cancer for newly diagnosed lung cancer cases enrolled by the Deep South CanCORS Consortium. Working closely with the Consortium, the special study will identify advanced lung cancer subjects (with tumor(s) inoperable for staging reasons), and follow them bimonthly by telephone until the subject's death or the end of the special study. Bimonthly follow-up is to include administration of at least two disease-specific instruments: The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Lung Cancer Specific Module (EORTC QLQ-LC13), which measures symptoms; and the Functional Assessment of Cancer Therapy lung cancer module(FACT-L), which assesses QOL. At least one general instrument is also proposed for use, SF-36, with physical functioning and role limitation subscales. Following the subject's death, staff will telephone and interview the nearest relative about the death using an investigator-developed, nineitem survey. Utilizing descriptive statistics and multi-variable models, investigators will test whether: African-Americans have lower QOL and worse symptom control than Caucasians; subjects with better symptom control have higher QOL; and subjects with higher QOL or better symptom control are more likely to die at home. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EXISULIND FOR CHEMOPREVENTION OF LUNG CANCER Principal Investigator & Institution: Bepler, Gerold; Program Leader, Profesor of Medicine, On; H. Lee Moffitt Cancer Ctr & Research Ins and Research Institute, Inc. Tampa, Fl 336129497 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant) Lung cancer is the leading cause of cancer death in the United States. Cure rates from primary treatment are low (approximately 15%). There is an urgent need to develop compounds, which can prevent the disease in individuals with a history of cigarette smoking and other factors associated with increased lung cancer risk. A number of compounds have been tested but trials to date have not resulted in a decrease of lung cancer incidence. In fact, two large-scale chemoprevention trials that evaluated beta-carotene in active and former smokers, resulted in an increase of incidence and mortality from lung cancer. Recently, the focus of lung cancer chemoprevention has shifted towards investigations using inhibitors of inflammatory response pathways and inhibitors of growth factor signaling pathways. A novel class of agents has been developed that induce apoptosis. Exisulind (Aptosyn) is the first agent in this class, and it has shown promise in chemoprevention of colorectal carcinoma by reducing the number of size of adenomatous polyps in humans. In animal
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studies, this agent has resulted in a reduction of carcinogen-induced lung cancer. To test the clinical utility of this agent in lung cancer prevention, we propose to perform a double-blind, placebo-controlled, randomized, clinical efficacy trial in former smokers. Participants will be stratified by lung cancer risk based on airway obstruction, prior history of completely resected stage I non-small cell lung cancer, and the histopathology of bronchial biopsies. They will be randomized 2:1 to drug vs. placebo. A surrogate marker of lung cancer, the proliferation marker Ki-67, will be used as the primary endpoint. Other markers previously and currently investigated by us and others (MCM2, hnRNP, apoptosis, cytokine response profiles, (epi) genetic alterations, morphology) will be explored as surrogate trial endpoints. Exisulind will be given orally at a dose of 500 mg daily for 6 months. With 93 evaluable participants randomized to exisulind, the study will have 80% power to detect a 50% or greater decrease in the mean Ki-67 labelling index as a result of treatment. Since we anticipate a 25% attrition rate, we are planning to enroll a total of 186 subjects over 4 years. Given the number of eligible subjects at our institution that already participate in early detection trials, we are confident that the goal of this proposed study can be achieved during the 5-years of funding. The data generated by these investigations will be important for future decisions on large-scale chemoprevention trials using disease incidence and mortality as endpoints. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENE EXPRESSION INDICES IN CHEMORESISTANT LUNG CANCER Principal Investigator & Institution: Willey, James C.; Professor; Medicine; Medical College of Ohio at Toledo Research & Grants Admin. Toledo, Oh 436145804 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-MAR-2004 Summary: Non-small cell lung cancer (NSCLC) is one of the most common causes of cancer death in this country and it is poorly responsive to current chemotherapeutic regimens with an overall regression rate of only 30-50 percent. Histological categorization provides extremely limited information regarding biological behavior of a particular NSCLC tissue. Progress in the genome project and advances in high throughput measurement of gene expression are providing the opportunity to re-define diagnosis of NSCLC tissues on the basis of important phenotypes, such as chemoresistance, rather than on the basis of histology. The primary long-term objectives of the proposed investigation are to improve mechanistic understanding of NSCLC chemoresistance and to develop a method for predicting which NSCLC tumors will respond. The mechanisms of resistance likely to involve multiple gene products. For example, in other studies it was determined that indices comprising multiple independent gene expressions values measured in bronchial epithelial cells correlated better than individual gene expression values when phenotypes for malignancy (c-myc x E2F-1/p21) and risk for lung cancer (GSTP1 x mGST x GSHPx). In preliminary studies, the H1435 non-small cell lung cancer (NSCLC) cell line is 50-fold more resistant to carboplatin than H460. Evaluation of 20 genes putatively associated with carboplatin chemoresistance using standardized mixtures of competitive templates in quantitative RT-PCR revealed that glutathione transferase (GST) p1, Bax alpha, GADD45, ERCC3, glutathione peroxidase and mGST genes are expressed at 100, 20, 10, 6, 5, and 4-fold higher levels respectively in H1435. These genes and other putative chemoresistance genes may be effectively combined into gene expression indices to produce a better marker for the chemoresistant phenotype. The over-all hypothesis of this proposal is that patterns of individual gene expression and/or indices comprising the expression
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values of multiple individual genes will provide an effective marker for chemoresistant NSCLC tumors. A National Cooperative Tumor Signature Group has assembled to test the hypothesis through completion of the following specific aims. AIM 1) Measure expression of putative chemoresistant genes in primary NSCLC tumor tissues then identify which, if any, correlate with resistant phenotype. AIM 2) Identify gene expression indices that correlate with NSCLC tumor chemoresistance AIM 3) Develop a standardized mixture of competitive templates that will allow inter-laboratory comparison of gene expression data. AIM 4) Automate the quantitative RT-PCR method. AIM 5) Develop an internet based databank for storage of the data acquired during this study and for storage of data acquired by other laboratories. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENETIC SUSCEPTIBILITY TO LUNG CANCER Principal Investigator & Institution: Christiani, David C.; Professor; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 10-APR-1997; Project End 31-JAN-2003 Summary: (Adapted from Applicant's Abstract). The leading risk factor for lung cancer in the U.S. is cigarette smoking. The incidence of lung cancer remains alarmingly high and, despite the use of modern diagnostic and treatment modalities, the overall cure rate is low. Thus, preventive efforts, based upon the understanding of risk factors may be of paramount importance in controlling this deadly disease. A minority of smokers develops lung cancer, suggesting variability in disease susceptibility. Smoking itself may contribute to a causal complex along with other contributing factors such as genetic predisposition. Moreover, only a small proportion of all cancers is explained by simple monogenic inheritance. Several polymorphisms in the genes responsible for either activation or deactivation of carcinogens have been reported to be associated with lung cancer risk. To date, however, no studies have had sufficient statistical power to examine a number of complex gene-environment interactions in lung cancer (e.g., dietary and occupational contributions or gene-gene interactions). A large molecular epidemiologic study is proposed to examine six polymorphic traits in metabolism and lung cancer risk and how this risk may be modified by dietary or occupational exposures. The application posits that the combination of traits which enhance activation of carcinogenic metabolites and decrease detoxification of reactive products will confer excess risk in current and former smokers. Furthermore, it suggests that this risk will be modified by diet and occupational exposures. It is intended that a better understanding of these risks and their modification could lead to more effective preventive strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETICS OF TOBACCO AND ALCOHOL RELATED CANCERS Principal Investigator & Institution: Brennan, Paul J.; World Hlth Org Intl Agcy Res on Cancer Int'l Agency for Res on Cancer Lyon, Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): Even though lung and upper aero-digestive tract (UADT) cancers are predominantly caused by tobacco and alcohol, only a minority of heavy smokers and heavy drinkers will develop lung or UADT cancer. A possible explanation for this is that the metabolisation of carcinogenic products, the level of internal dose and subsequent DNA repair and cell cycle control mechanisms vary
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widely between individuals because of genetic factors. The broad long-term goal of this project will be to investigate in two separate studies the role of 45 genes which are potentially involved in the susceptibility of lung and UADT cancers. The first is a study of lung and UADT cancers in Central Europe, involving approximately 2300 lung cancer cases, 1200 UADT cancer cases and 2800 controls. The second is a separate study of UADT cancer in South America involving approximately 2100 cases and 1700 controls. Both studies are conducted to an identical protocol involving the collection of high quality detailed information on lifestyle and occupational history, as well as blood collection for DNA extraction. Genotyping of 108 SNPs for the 45 genes will be conducted using automated and pre-validated DNA microarrays. The genes comprise those involved in the metabolism of tobacco products, alcohol and other potential carcinogens (e.g. CYPs, GSTs, ADH2, ADH3, MPO), as well as genes involved in DNA repair (e.g. XRCC1, XRCC3, XPD, XPF), tumour suppression (p53, p16, CCND1 ) and nicotine addiction (dopamine D2 and D4 receptor genes). Using these large sample sizes, we will accurately measure the overall effect of each gene in lung and UADT cancer. Subsequently, the effect of combinations of genes will be measured (gene-gene interaction), as well as the effect of individual genes in specific subgroups identified by alcohol and tobacco consumption and occupational history (gene-environment interaction). Statistical techniques will include haplotype reconstruction, empirical Bayes and semi-Bayes analysis to control for false positive results, and modeling of complex pathways. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: HEDGEHOG PATHWAY INHIBITION BY CYCLOPAMINE IN CANCER Principal Investigator & Institution: Watkins, D Neil.; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Lung cancer results in more deaths than colon, breast and prostate cancer combined. Conventional cytotoxic therapy of lung cancer is limited by side effects, and is rarely curative. Mechanism based therapies directed at tumor specific pathways offers hope for the development of novel treatments. With this in mind, we have studied activation of mammalian development pathways in human lung cancer to provide insights into how such interventions can be achieved. The morphogen sonic hedgehog (Shh), which signals to adjacent embryonic cells to specify morphogenic patterns and progenitor cell fates, is essential for lung development. In extensive preliminary studies, we provide compelling evidence that many human lung cancers activate Hedgehog (Hh) signaling. We demonstrate cell autonomous Hh signaling in small cell lung cancer (SCLC), whereas non-SCLC (NSCLC) sends a Shh signal to adjacent stromal cells. Moreover, we find that specific inhibition of Hh signaling by the Veratrum alkaloid cyclopamine inhibits the growth of SCLC cells exhibiting pathway activation both in vivo and in vivo. Although NSCLC cells express Shh, they are not sensitive to cyclopamine and do not demonstrate cell autonomous pathway activation in vivo. However, NSCLC cell lines which signal to adjacent fibroblasts in vivo are growth inhibited by cyclopamine in vivo, suggesting that tumorstromal interactions mediated by Shh promote malignant growth. These data show that activation of the Shh pathway promotes the malignant behavior of lung cancer, and that inhibition of this pathway may represent a novel mechanism-based therapy. Outside of studies in CNS tumors, this is the first direct demonstration of Hh pathway activation in any human cancer. Moreover, our studies show that this phenomenon is not a general
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feature of carcinomas, but is restricted to epithelial systems in which Hh signaling plays a role in development. We propose to establish inhibitors of Hh signaling as clinically useful therapies in lung cancer using an approach integrating human tumor tissue arrays, molecular and cell biology studies, mouse models and basic pharmacology. First, we will identify the prevalence of Shh pathway activation in lung cancer and premalignant airway tissue using immunohistochemical markers. Then, using genetically engineered reporter cell lines and mouse models, we will study the pharmacologic effect of Hh pathway inhibitors on tumor growth, pathway activation and tumor-stromal interactions. Using these preclinical models, we will then perform delivery, dosing and toxicity studies as a rational basis for eventual phase one studies in humans. This research plan will firmly establish the importance of Shh signaling in lung cancer, and provide a rational, mechanism based approach for the treatment of lung cancer with inhibitors of the Shh pathway. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: HSP110-LUNG TUMOR ANTIGEN COMPLEX AS A CANCER VACCINE Principal Investigator & Institution: Subjeck, John R.; Professor; Corixa Corporation 1124 Columbia St, Ste 200 Seattle, Wa 98104 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JAN-2004 Summary: (provided by applicant): The objective of the research is to develop an effective vaccine for the treatment of lung cancer. The commercial value derives from the novelty of the lung cancer antigen, L523S, as well as the novelty of the molecular chaperone approach using hsp110. L523S is expressed in a large number of lung carcinomas and has been shown to be immunogenic. Hsp110 is a heat shock protein with strong chaperoning properties. This molecular chaperone is then naturally complexed with L523S by heat shock. Since heat shock proteins have natural immunological functions, this hsp110-L523 S vaccine may well provide an effective therapy in the treatment of lung cancer and correspondingly have significant commercial value. Two specific aims are defined. Aim 1 will be to manufacture active, recombinant hsp110 in large quantity, establish its chaperone and immune activity, and then to verify its proper binding to the 523S lung cancer antigen. Aim 2 will determine the ability of the hsp110-L523S natural chaperone complex to elicit antigen specific immune responses in mice and will compare the magnitude of these responses to conventional approaches. Effective vaccines against lung cancer have not been previously developed and the characterization of this approach could lead to highly marketable commercial product. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IDENTIFYING GENES THAT CAUSE LUNG CANCER TO PROGRESS Principal Investigator & Institution: Debs, Robert J.; Senior Scientist; California Pacific Med Ctr-Pacific Camp San Francisco, Ca 94115 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Recently, cDNA microarray studies have identified multiple different genes that are aberrantly-expressed in aggressive human lung cancers. However, to translate these microarray-based results into improved therapies for cancer patients, the critical genes whose aberrant expression actually controls metastatic spread must now be identified. To date, functional assays for identifying such
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metastasis-controlling genes have been limited. Systemic gene transfer in adult, tumorbearing mice is a powerful new approach to this problem. We now propose to use new systemic gene transfer technologies to identify which of nine selected genes (already identified by cDNA microarray studies to be aberrantly-expressed in poor prognosis, primary human lung cancers) actually control the metastatic spread of two different murine lung cancer tumor lines, LLC-LM and LLC-HM, in tumor-bearing mice. Our three specific aims are: Aim 1: To maximize the level and duration of gene expression produced in tumor-bearing mice by PEI- and IV, CLDC-based gene delivery. We will identify the most efficient, durably-expressing systemic gene transfer approaches for transfecting LLC-LM and LLC-HM cells in tumor-bearing mice. To accomplish this, we will optimize the: A) DNA carrier system, B) plasmid DNA:carrier ratio and C) repetitive dosing schedule. Aim 2: To use systemic delivery of selected cDNAs and ribozymes to identify specific genes that control the metastatic spread of lung cancers in mice. We will identify specific genes whose blocked expression or over-expression significantly reduces the metastatic spread of LLC-LM and HM in mice. Specifically, we will use plasmid-based ribozymes to target the endogenous expression of the CD98, cathepsin L, prostaglandin E synthase or VEGF-C genes, and use plasmid-based cDNAs to over-express the p21, 14-3-3, TGF-beta, thymosin beta or diacylglycerol genes. Each of these nine genes has already been identified by cDNA microarray studies to be aberrantly-expressed specifically in poor prognosis human lung cancers, and has been linked to the malignant phenotype. Aim 3: To identify pairs of metastasis-controlling cDNAs and/or ribozymes that act synergistically. We will assess IV co-injection of pairs of plasmid-based ribozymes and/or cDNAs that produce significant metastasiscontrolling effects against murine lung cancer lines in Aim 2. We will assess multiple different dose combinations of each pair tested to determine whether there are specific interactions between each pair of genes. Overall, we will attempt to identify specific genes whose altered expression is functionally required for the metastatic spread of lung cancers. These critical metastasis-controlling genes can be specifically targeted by emerging small molecule-, protein- and gene-based therapeutic approaches; including those based on the more powerful systemic gene transfer approaches we have recently developed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: IMAGING MDR CHEMOTHERAPY EFFECT IN SMALL CELL LUNG CANCER Principal Investigator & Institution: Piwnica-Worms, David; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 31-MAY-2002; Project End 31-MAR-2007 Summary: (provided by applicant): Lung cancer is the leading cause of cancer related death in the United States. Approximately 20% of patients with newly diagnosed lung cancer have the small cell histological type (SCLC). Even though it is more responsive to chemotherapy, nearly all patients with extensive stage small cell lung cancer succumb to recurrent disease. Overexpression of the multidrug resistance gene (MDR1) and its protein product P-glycoprotein (Pgp) as well as the multidrug resistance-associated protein-1 (MRP1) have been shown to result in poor response to therapy and shorter survival in SCLC when compared to those whose tumors do not overexpress these MDR determinants. Because many of the drugs in current use are impacted by Pgp and MRP1 (i.e., etoposide, paclitaxel, anthracyclines, vincristine), it is conceivable that administration of these chemotherapeutic agents may contribute to the emergence of drug resistance clones, ultimately contributing to poor outcomes. Thus, functional
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identification of Pgp, and perhaps MRP1, at the time of presentation could provide important information which could direct the choice of chemotherapeutic options. We have discovered that Tc-99m-Sestamibi, a commercially available radiopharmaceutical, is recognized as a transport substrate by the human MDR1 P-glycoprotein in vitro and in vivo and may be recognized by MRP1. Thus, Tc-99m-Sestamibi may serve as a molecular imaging agent enabling functional identification of transporter-mediated resistance by scintigraphy. However, single photon agents such as Tc-99m-Sestamibi, while yielding high quality images for analysis of superficial tissues such as breast tumors, are prone to attenuate artifacts when applied to lesions deep in the thorax such as lung tumors. At Washington University, the cyclotron Research Resource can produce a variety of non-standard isotopes, including Tc-94m, a novel isotope suitable for positron emission tomography (PET). Thus, the WU ICMIC has an unique opportunity to directly translate our extensive biochemical and clinical experience with Tc-99m-Sestamibi imaging of MDR into novel PET studies with Tc-94m-Sestamibi. Exploiting the quantitative advantages of PET in this project, we propose to use Tc-94mSestamibi PET to image patients with extensive stage SCLC. We propose to test the hypothesis that dynamic imaging of lung tumors with Tc-94m-Sestamibi will predict treatment failure in patients with extensive stage small cell lung cancer and determine whether Pgp and MRP1 together or independently impact Tc-94m-Sestamibi pharmacokinetics in lung tumors in vivo. Molecular imaging of the MDR phenotype with radiopharmaceuticals may provide a novel tool to rapidly characterize clinically relevant MDR in human tumors in vivo, target MDR modulators in vivo, and ultimately provide a means to direct patients to molecular-specific cancer therapies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: IMPACT OF SMOKING ON LUNG CANCER CHEMOPREVENTION Principal Investigator & Institution: Hong, Waun K.; Professor and Chairman; Head Neck & Thoracic Med Oncol; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 20-AUG-2001; Project End 31-JUL-2006 Summary: (provided by applicant) Lung cancer is the leading cause of cancer death among both men and women in the United States today, and a rising public health problem throughout the world. Although we?ve seen some improvement using combined modality approaches, these have had little impact on survival. Chemoprevention is a highly promising new approach that has already shown enormous potential for the control of other epithelial solid tumors. However, numerous studies of lung cancer chemoprevention have shown no benefit, and some have shown actual harmful effects in current smokers. It seems clear that previously unsuspected adverse interactions exist between tobacco carcinogens and chemopreventive agents. Although further studies of lung cancer chemoprevention are warranted, a thorough investigation of these carcinogen/chemoprevention interactions is necessary before further large-scale randomized trials are implemented. The overall goals of this translational, multidisciplinary Program project are to elucidate the interactions between tobacco carcinogens and chemopreventive agents, investigate the potential of celecoxib for lung cancer chemoprevention, and validate intermediate markers of lung carcinogenesis. To accomplish our goals, we propose to carry out a clinical chemoprevention trial in humans, while performing genetic, molecular, and pharmacologic studies to understand the carcinogenic process and the interaction of carcinogens with chemopreventive agents through the following projects: Project 1: Clinical Trial of Celecoxib in Lung Cancer Chemoprevention Project 2: Lung Cancer
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Prevention by COX-2 and 5-LOX Inhibitors, Retinoids, and Their Combinations Project 3: Molecular Alterations in Lung Carcinogenesis Project 4: The Role of Transcription Factor NF-kB in Lung Cancer Development and Chemoprevention Core components (Administration, Biostatistics and Data Management, Histology, and Pharmacology) are also included to provide the structure and expertise required for the successful integration and execution of these studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: INTERNATIONAL CONFERENCES ON SCREENING FOR LUNG CANCER Principal Investigator & Institution: Henschke, Claudia I.; Professor; Radiology; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2004 Summary: (provided by applicant): The first study of the Early Lung Cancer Action Project (ELCAP), led by Dr. Caludia Henschke, Ph.D., M.D. of the Weill Medical College of Cornell university and New York) Presbyterian Hospital, demonstrated that annual low-dose chest computed tomography (CT) screening has the potential to markedly increase the diagnosis of small, early stage lung cancers. With such early diagnosis, the cure rate of individuals with lung cancer has been greater than 70%. As a result of the worldwide interest in CT screening for lung cancer, we held our initial conference entitled the "International Conference on Screening for Lung Cancer." It was partially supported by an NCI conference grant. We invited all investigators from around the globe involved in ongoing screening studies as well as those with proposed studies. We also invited participants to discuss imaging and molecular diagnostics for early detection of lung cancer, as well as innovative treatments and chemoprevention. Study design issues and health care policies are addressed in depth, offering the opportunity for medical professionals to exchange ideas and to collaborate on research activities. To date, six semi-annual conferences have been held with an enrollment totally more than 1200 participants. The increasing enrollment at each successive conference demonstrates that, in a short time, these conferences have become an important forum for lung cancer screening specialists. The broadest mission of these semi-annual conferences is the collective pursuit of avant-garde understanding of the issues surrounding early diagnosis and early treatment of lung cancer. Any given Conference focuses on issues that are particularly topical at the time. Lectures are devoted to these issues on one day with workshops being held on the second day and the development of a consensus on these issues during the third day. The consensus statement and particulars of the workshops are then published on the ICScreen.med.cornell.edu website. These conferences are open to all. At each conference we provide an update on the interim advances in both research and practice of early diagnosis and early treatment as well as an update on the results of screening trials, whether they are randomized controlled trials or not. We also review the progress of all collaborating worldwide institutions. New technologies and methodologies are continually being developed to refine measurements, data collections, and statistical evaluations, all of which are aimed at promoting further reductions in lung cancer morbidity and mortality. All viewpoints and types of methodologic issues inherent in screening evaluation are openly discussed by invited experts. As a result of the conferences, critical issues which might require further study will be addressed. Consensus reports will be developed. The advantage of such a consensus reports is that it will provide useful and up-to-date information about CT screening on which to base the national and international policies in a very timely and cost-efficient manner.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: IOWA AND MISSOURI RADON LUNG CANCER STUDIES Principal Investigator & Institution: Field, Robert W.; Epidemiology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 17-JAN-2001; Project End 31-DEC-2005 Summary: Risk estimates, extrapolated from studies of underground miners, predict that residential radon progeny exposure accounts for approximately 19,000 lung cancer deaths each year in the United States. Previous case-control epidemiologic studies, which examined the relationship between residential radon exposure and lung cancer, lacked the ability to verify these risk estimates. Inaccurate dose assessment of radon exposure, a high percentage of proxy respondents, inadequate pathologic review, and low residential radon concentrations led to exposure misclassification and limited the interpretation of these studies. The Iowa Radon Lung Cancer Phase I study was designed to overcome many of these limitations. The Phase I study utilized advanced radon dose assessments, independent histologic review, and a study population that was characterized by geographic stability, high percentage of live cases, and potential for high radon exposure. The Phase I study demonstrated that exposure to residential radon gas increases the risk of developing lung cancer. To refine these estimates, we now propose Phase II studies that examine the association between residential radon product (progeny) exposure and the development of lung cancer. Because radon progeny deliver the actual radiation dose to the lung tissues, rather than radon gas itself, in order to reduce further the exposure misclassification, radon dose estimates need to take into account exposure to residential radon progeny. This requires measuring actual airborne radon progeny concentrations and integrating the exposure to radon progeny over time. The Phase II study will derive more accurate retrospective radon dose estimates by using a novel retrospective radon progeny integrating glass-based detector. Specific Aim I examines the hypothesis that exposure to residential radon progeny is associated with increased risk of developing lung cancer, after controlling for confounders. We will perform field calibration and laboratory validation of the retrospective radon "glass" detectors, and analyze the risk estimates by incorporating exposures to radon progeny, rather than exposures to radon gas. Specific Aim II will determine whether the shape of the dose response curve that best describes the relationship between residential radon progeny exposure and lung cancer risk is linear or nonlinear. Specific Aim III will examine whether exposure to radon progeny contributes to the development of adenocarcinoma, as well as other lung cancer histologic types. For Aims II and III we will use pooled analyses of exposure estimates that are derived from retrospective radon progeny "glass" detectors for subjects from the Iowa and Missouri Radon Lung Cancer Studies. The pooling of data between two largescale epidemiologic studies from a similar geographic area, Iowa and Missouri, will allow us to increase sample size and statistical power. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LOCALIZED VITAMIN DEFICIENCIES AND RISK FOR LUNG CANCER Principal Investigator & Institution: Piyathilake, Chandrika J.; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-JUN-1997; Project End 31-MAY-2003
30 Lung Cancer
Summary: (Applicant's Description) Although there is substantial epidemiological and experimental evidence of a protective effect of a high intake of fruits and vegetables against lung cancer (LC), studies that have attempted to isolate specific nutrient effects have given variable results. One possible reason for the lack of consistency between studies of individual nutrients and fruits and vegetables is that the frequently studied components like beta-carotene and other antioxidants in fruits and vegetables may not be the only protective components. We advance the possibility that folate in fruits and vegetables is one of these relatively unstudied components. The potential mechanisms whereby deficiencies of folate and inter-related vitamin B-12, could lead to gene damage via DNA hypomethylation are well understood. Furthermore, chemical components of cigarette smoke have been shown to interact with folate and vitamin B-12, transforming them into biologically inactive compounds. That these chemical reactions may have physiologic significance is supported by the reports of lower circulating and buccal mucosal folate levels in smokers, and a response of bronchial metaplasia to folate/B-12 supplementation. We expect the effect of smoking to be greatest in the lung, where the potential for cigarette smoke to oxidize and destroy micronutrients should be most pronounced. Yet, the importance of folate and vitamin B-12 in LC prevention is not widely appreciated. There are no reports on the measurement of folate or vitamin B-12 levels in lung tissue. Although there are some reports on the epithelial lining fluid (ELF) levels of vitamins C and E, and their accumulation by alveolar macrophages (AM) of smokers, none of these studies has measured a battery of vitamins in the same sample, studied the significance of AM accumulation of vitamins, or most importantly, correlated those vitamins with the expression of intermediate endpoint biomarkers (IEB). The identification of IEB in LC has proceeded briskly, but studies of the chronology of early events are only in their infancy. Therefore, special emphasis will be given to the identification and validation of IEB in lung carcinogenesis since this is an inadequately documented but emerging area in cancer prevention research. This fiveyear Preventive Oncology Academic Award will provide the applicant with intensive training in IEB research under expert guidance to become an independent researcher in this area. Following this, the dietary intake and concentrations of folate, vitamins B-12, A, E, C, and beta-carotene in ELF, AM, bronchial biopsies, and blood will be measured along with global DNA hypomethylation and IEB in bronchial biopsies of smokers and non smokers matched for age, gender, and race. Along with identifying and validating IEB, the proposed studies will provide insight into the mechanisms for the welldocumented protective effects of fruits, vegetables, and antioxidant nutrients on the risk for lung cancer in smokers, and will provide much needed base-line data for the evaluation of chemopreventive applications of vitamins. These activities, along with advanced studies of epidemiology and statistical analysis and experience in teaching, will provide the expertise needed for a career as a successful, independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LUNG CANCER Principal Investigator & Institution: Jett, James; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 01-JAN-1982; Project End 31-DEC-2005 Summary: Between 170-250 patients per year were enrolled on lung cancer treatment trials between January, 1996, and December, 1999. Additionally, 200 patients were enrolled on ancillary trials, as well as quality of life and cancer control trials. During this grant cycle, we have published 11 abstracts and 12 manuscripts related to NCCTG trials. Six other manuscripts are in preparations. Three major accomplishments were made
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over this period: First, we have complete two phase III randomized trials with combined modality therapy that have evaluated the role of twice daily hyperfractionated radiotherapy. In these trails, patients received concurrent chemoradiotherapy. One trail was in small cell (SCLC) and the second in non-small cell lung cancer (NSCLC). These were important trials for scientifically evaluating hyperfractionated radiotherapy. Additionally, these trials further evaluated the evaluated the risks and benefits of concurrent chemoradiotherapy. We have learned that acutely concurrent therapy is somewhat more toxic, but tolerable, and results in improved survival for small cell lung cancer. However, hyperfractionated radiotherapy, when given with cycle 4 of chemotherapy, did not impact on survival versus concurrent chemoradiotherapy with once a day irradiation. The results of the impact on survival versus concurrent chemoradiotherapy with once a day irradiation. The results of the impact on survival versus concurrent chemoradiotherapy with once a day irradiation. The results of the impact on survival versus concurrent chemoradiotherapy with once a day irradiation. The results of the non- small cell lung cancer trial are pending. The small cell trial has resulted in a change in practice in the community with concurrent therapy becoming the standard. Second, our community-based oncologists and thoracic surgeons have successfully completed a neoadjuvant chemotherapy trial in early stage (stage I and II) lung cancer and participated in an adjuvant trial for resected stage II and IIIA non-small lung cancer. We have learned that neoadjuvant chemotherapy does not increase surgical morbidity and/or mortality. These trials have prepared us for participation in the current neoadjuvant phase III Intergroup trial (S9900) in early stage patients and Intergroup adjuvant trials in totally resected patients with more advanced disease. Third, new chemotherapy gents and combinations (LU103793, topotecan/paclitaxel topotecan/cisplatin) were tested in NSCLC and found not to be effective or associated with excessive toxicity. These are important negative findings. Additionally, topotecan/paclitaxel alternating with etoposide/cisplatin has been tested against small cell lung cancer with promising results. NCCTG was also a major contributor to the Intergroup surgical adjuvant trial for resected stage II/IIIA NSCLC (INT 0115). Future Plans. A new leadership team is now in place, and the group is focused on building on its strengths to advance the treatment of lung cancer. Accrual on phase III trials has not been adequate to conduct Phase III trials sorely within NCCTG in a timely fashion. Treatment trials within NCCTG in the next grant cycle will, therefore, be primarily phase II studies testing the role of novel chemotherapy agents and agents that will, therefore, be primarily phase II studies testing the role of novel chemotherapy agents and agents will target specific abnormalities. We will focus on novel agents that affect signal transduction pathways. Promising treatments will be brought forth for rapid testing in large phase III studies in the Intergroup setting. In addition to selected ancillary studies with treatment trials, translational research in the genetic epidemiology of lung cancer will be an area of emphasis. The third area of research will be the treatment of lung cancer in the elderly, who are increasingly represented in our patient population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LUNG CONSORTIUM--IOWA
CANCER
CARE
OUTCOMES/SURVEILLANCE
Principal Investigator & Institution: Wallace, Robert B.; Professor; Epidemiology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 20-SEP-2001; Project End 31-AUG-2006
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Summary: We have assembled a team of multi-disciplinary investigators to study, on a population basis, the patterns of treatment initially and continuing for a representative sample of lung cancer patients in the state of Iowa. These patterns will be explored in terms of patient decision-making processes for short and long-term treatment, with follow-up for suitable outcomes including disease-free interval, quality-of-life measures, end of-life care and overall survivorship. Factors proposed for exploration include including patient demographic, economic and behavioral attributes, including traits such as the patient's cancer learning environment and fatalism, the influences of geographically-dispersed practitioners with varied clinical management approaches, practitioner continuing education and information sources, the application of treatments where optimal approaches are uncertain and the influence of spatial and fiscal access to care. Special features of this proposal include: a) a multi-disciplinary team of investigators including epidemiology, disease registration, biostatistics, health economics, behavioral science and thoracic oncology; b) proven ability to access approximately 2000 lung cancer patients per year and achieve long term follow-up rates of 98-99%, using the Iowa Cancer Registry (NCI SEER Program); c) the elaboration of an economics model to guide both theory and questionnaire design for patients and practitioners, and offered to understand patient decision-making and its relation to outcomes; and d) demonstrable high levels of community cooperation, from patients, cancer care practitioners and pathologists. The goal of the special study is to use Instrumental Variable (IV) techniques to assess whether patient survival rates can be increased by increasing adjuvant therapy treatment rates for early stage non-small cell lung cancer (ENSCLC) patients. If providers are accurately sorting patients by their expected treatment benefits, and only patients expected to benefit from adjuvant treatments actually receive them, we would expect that treatment benefits for patients on the extensive margin to be minimal. We hypothesize there will be little or no treatment survival benefits for patients on the ENSCLC patients provides the rationale for this study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LUNG PREVENTION
CANCER
IN
THE
US:
PATHOGENESIS,
TRENDS,
Principal Investigator & Institution: Moolgavkar, Suresh H.; Professor; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2002; Project Start 10-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant)Using the SEER database, which covers more than 10% of the US population, lung cancer incidence trends over the period 1973-1998 will be investigated using extensions of age-cohort-period models. Specifically, it is proposed to develop models in which non-specific age effects are replaced by parametric hazard functions that acknowledge the multistage nature of carcinogenesis. At least formally, this procedure finesses the well known problem of arbitrary linear trends that plagues the traditional age-cohort-period models. Furthermore, analyses of carefully collected incidence data in large registries such as SEER using biologicallybased modelscan lead to insights in to the mechanisms underlying carcinogenesis in addition to shedding light on temporal trends. With respect to temporal trends, attempts will be made to relate trends in lung cancer incidence to trends in smoking habits in the US. Tobacco smoke contains both mutagens and agents that impact cell proliferation kinetics. Thus, tobacco smoke probably acts as both an initiator and a promoter in lung carcinogenesis. One goal of these analyses is to investigate whether non-specific and birth cohort and calendar year trends can be directly linked to specific
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aspects of carcinogenesis, such as initiation, promotion and progression. This possibility will be investigated by incorporating tobacco consumption trends into the parameters of the multistage model. Because of the large size of the SEER database it should be possible to conduct these analyses separately by race, sex and histologic type. Finally, the estimated parameters of the optimal multistage model will be used to project lung cancer incidence trends into the future under various assumptions regarding changes in composition of cigarettes and smoking habits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LUNG CANCER--ROLE OF PTHRP AND REGULATION BY TGFBETA Principal Investigator & Institution: Tannehill-Gregg, Sarah H.; Veterinary Biosciences; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: (Applicant's Description): The overall goal of the K08 award is to permit Sarah Tannehill-Gregg, D.V.M. to devote full time for research training leading to a Ph.D. in experimental pathobiology, and for development into an independent scientist for a cancer in academia or biomedical research. Dr. Tannehill-Gregg has completed a residency in comparative pathology and one year of research training in the sponsor's laboratory. The research goals are to investigate the regulation of extracellular calcium and the role of transforming growth factor-beta in parathyroid hormone-related protein (PTHrP) expression and secretion by cancers of the lung. This will address an important medical question since PTHrP is expressed by many carcinomas and is responsible for inducing humoral hypercalcemia of malignancy. The action of TGFbeta may be a critical determinant in the overexpression of PTHrP by carcinomas and play an important role in the pathogenesis of cancer-associated hypercalcemia in human patients. The overall hypothesis to be tested is that TGFbeta production by lung carcinoma acts as an autocrine or paracrine against to stimulate PTHrP production by the carcinoma cells. Aim 1: Investigate expression of PTHrP, TGFbeta1-3 and TGFbeta receptors (I and II) and measure serum ionized calcium and PTHrP concentrations and urine excretion of calcium and phosphorus in humans with lung cancer. Aim 2: Investigate the regulation of PTHrP expression and secretion by TGFbeta in lung carcinomas in vitro using explant cultures from spontaneous human neoplasms and cultures of lung carcinoma cell lines. Aim 3: Investigate the molecular regulation of PTHrP mRNA steady state levels, stability, and alternate splicing by TGFbeta in vitro using lung carcinoma explants and cell lines. Dr. Tannehill-Gregg has developed preliminary data to support all three aims and a collaboration with Medical and Surgical Oncology to facilitate the in vivo studies. The cooperative efforts of Dr. Tannehill-Gregg, the sponsor, and co-investigators in the Department of Veterinary Biosciences, Comprehensive Cancer Center, James Cancer Research Hospital, Pulmonary Oncology and Thoracic Surgery Divisions, and Tissue Procurement Program at Ohio State University will provide a productive environment to complete this significant investigation. The studies will provide important new data on the function of PTHrP and TGFbeta in lung cancer in human patients. The combination of results from in vivo study, in vitro cultures, and mechanistic molecular experiments will contribute to the understanding of the role of PTHrP in lung cancer and provide insight into the pathogenesis of cancer-associated hypercalcemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NETWORK
LUNG/COLON
CANCER
OUTCOMES--CANCER
RESEARCH
Principal Investigator & Institution: Weeks, Jane C.; Assistant Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 18-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): We will accrue all patients with newly diagnosed lung or colon cancer receiving their care in one of five geographically diverse sites in the Cancer Research Network, an NCI-funded research consortium of HMOs. Automated data for all patients (2,058 patients with lung cancer over the two year enrollment period, and 1,732 patients with colon cancer over the two year enrollment period) will be supplemented with data obtained from complete medical record review and patient surveys for a sample of 1,424 patients with newly diagnosed lung cancer and 1,222 patients with newly diagnosed colon cancer. We will oversample African-Americans, Asians and Pacific Islanders, as well as Medicaid recipients. In addition, we will assemble an inception cohort of patients with newly diagnosed metastatic recurrences of colorectal cancer during the two-year enrollment period (projected at approximately 300 patients) for comprehensive data collection. We propose to lead analyses of CanCORSwide core data in order to (1) examine the effect of race and ethnicity on patterns of care, treatment choice, quality of life, symptom control, and satisfaction; (2) characterize the types of providers seen by patients and examine the associations between provider characteristics/attitudes and patterns of care and outcomes; (3) evaluate the relationship between the structure/function of cancer care in the health care delivery systems of participating patients and patient outcomes, including health status, patient satisfaction, and cost; and (4) generate estimates of utility weights and time- and out-of-pocket costs that are disease- and treatment-specific for use in future cost-effectiveness analyses. Finally, in a Special Research Study we will aggregate cost data for CRN CanCORS subjects in order to (1) determine cancer-attributable phase-specific and lifetime costs of care for colorectal and lung cancer; (2) determine the proportion of total cancerattributable costs that are spent on initial therapy versus second- and third line therapies for each cancer, stratified by stage at diagnosis; and (3) determine the relationship between type of initial therapy and the subsequent lifetime cancer-attributable costs of care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MATRIX METALLOPROTEINASES IN LUNG CANCER Principal Investigator & Institution: Matrisian, Lynn M.; Professor and Chair; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): Matrix metalloproteinases (MMPs) have been implicated in tumor growth, angiogenesis, invasion, and metastasis. There is extensive preclinical data that inhibition of MMP activity results in a reduction in tumor burden and prolongs the survival of treated animals. Synthetic MMP inhibitors (MMPIs) are currently in Phase III clinical trials in a variety of tumor types, and non-small cell lung cancer (NSCLC) trials in particular have been initiated with several different compounds. The results of the initial studies with the broad spectrum inhibitor marimastat (British Biotech) showed little benefit in advanced pancreatic and gastric cancer, but encouraging results in patients without overt metastases. Studies with the MMPI tanomastat (Bayer Corp.), however, were stopped when preliminary results from an adjuvant small cell lung cancer (SCLC) trial demonstrated that the MMPI was
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performing worse than placebo. These results raised the realization that very little is known about the role of MMPs in lung cancer development and progression. This proposal is designed to test the hypothesis that MMPs are valid therapeutic targets for lung cancer, and to determine the MMP family members that represent the most appropriate targets for MMPIs in NSC and SC lung cancer. The following specific aims are proposed: 1) Determine the expression profile of MMP transcripts and protein in SCLC and NSCLC samples and associate the expression profile with response to MMPI treatment. 2) Determine if MMPIs inhibit MMP activity in lung cancer patients using an ex vivo MMP activity assay, and 3) Determine the efficacy of MMPIs in chemicallyinduced and orthotopic preclinical models of lung cancer. The availability of mice that are null for several MMP family members provides the opportunity to examine the role of specific MMP family members in these model systems. These studies represent translational research that will guide the selection and application of selective MMPIs to the treatment of lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MODELING INTERVENTIONS FOR LUNG CANCER MORTALITY Principal Investigator & Institution: Holford, Theodore R.; Professor; Epidemiology and Public Health; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 15-AUG-2002; Project End 31-JUL-2006 Summary: (provided by applicant)The study of time trends in cancer incidence and mortality can provide valuable insights into the effect that a disease is having on the population. A model will be developed in which the effect that smoking cigarettes, a well know cause of this disease, has on population based lung cancer rates. Age-periodcohort models have offered one useful way of developing a statistical summary of temporal trends. In this case, age represents the effect of the aging process on a disease risk. Period and cohort, on the other hand, are likely to reflect changes in the exposure to import risk factors or in the surveillance system. While analytical epidemiologic studies offer the best way to estimate the effect of putative risk factors on disease risk, quantitative descriptions of the way in which changes in exposure can affect population rates can be much more challenging. The purpose of this research is to develop a model in which trends in risk factors for lung cancer incidence are used to describe observed trends in incidence and mortality for the disease. These will then be used to estimate the effect on lung cancer mortality of interventions designed to reduce cigarette smoking. The specific aims of this research are to: 1. Develop a model for lung cancer incidence trends among SEER registries and determine the extent to which available data on smoking trends can be used as explanatory variables; 2. Develop a compartment model that describes the relationship between lung cancer incidence and mortality using available data from SEER registries; 3. Develop a model that uses available state information on cigarette smoking trends to explain the variation in cancer mortality trends among contiguous states; and, 4. Use the model developed in aims1-3 to estimate the population effect of various anti-smoking campaign strategies on future lung cancer mortality trends. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MODELING LUNG CANCER IN TELOMERASE NULL MICE Principal Investigator & Institution: Wong, Kwok-Kin; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008
36 Lung Cancer
Summary: (provided by applicant): Lung cancer is a major international health problem. In the United States alone, an estimated 157,000 people will die of this disease in 2001 and tobacco use accounts for 85% of all lung cancers. Despite recent advances in cytotoxic drug development, radiotherapy and surgical management, the cure rate for advanced lung cancer remains poor. Further, much remains unknown about the molecular and genetic events involved in initiation and progression of lung cancer. One important mechanism seen in the development of epithelial cancers (i.e., lung cancer) appears to be underlying chromosomal instability due to a loss in telomere function brought about by significant cell division in the face of insufficient telomerase activity. Our laboratory has proposed that a combination of age-dependent epithelial renewal, somatic mutations that drive clonal proliferation, and chronic injury can accelerate telomere erosion, this culminating in a chromosomal fusion-bridge-breakagetranslocation process. This process provides a mechanism for rapid and wholesale changes in cells, with rare cells incurring a threshold number of relevant changes to initiate the transformation process. Reactivation of telomerase or upregulation of alternative telomere maintenance mechanisms restabilizes the genome, allowing such initiated cells to expand and acquire changes resulting in a fully cancerous cell. I propose to build on the unique experimental attributes of the telomerase deficient mouse to develop a lung cancer model that is driven by mechanisms underlying the genesis of human lung cancer. A physiologic mouse model of lung cancer may be developed by exposing the telomerase deficient mice with shortened telomeres to chronic tobacco smoke: this will accelerate lung epithelial cell turnover and promote genome wide mutagenesis. Once validated, this model will be used to examine the role of telomerase activation during carcinogenesis, and as a tool for novel lung cancer gene discovery. The applicant is an M.D. who will have completed a residency in internal medicine with subspecialty training in adult medical oncology prior to the proposed start date. He also holds a Ph.D. in molecular biology and biophysics. The proposed research will be carried out in the laboratory of Dr. Ronald DePinho at the Dana Farber Cancer Institute. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MODELING LUNG CANCER: RISKS, PROGRESSION, AND SCREENING Principal Investigator & Institution: Kimmel, Marek; Professor; Statistics; Rice University 6100 S Main Houston, Tx 77005 Timing: Fiscal Year 2002; Project Start 18-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): We propose to construct a realistic statistical model of lung cancer risk and progression that will make it possible to relate current trends in lung cancer incidence and mortality to past trends in smoking in the US population. We depart from existing approaches by having the model include genetic and behavioral determinants of susceptibility, progression of the disease from precursor lesions through early localized tumors to disseminated disease, detection by various modalities, and medical intervention. Using model estimates as a foundation, we intend to predict mortality reduction caused by primary prevention, and early-detection and intervention programs, under different scenarios. This includes utilization of genetic indicators of susceptibility to lung cancer to define the highest-risk subgroups of the high-risk behavior population (smokers). To allow for uncertainty in the various sources of data we will develop parameter estimation techniques using simulation and Bayesian hierarchical modeling approaches. Along with developing new methodology, we will apply our techniques to a variety of data sets available to us, which will allow
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calibration and validation of the model. To investigate and develop lung cancer susceptibility, we will use tobacco impact estimates developed at the University of California at San Diego, as well as case-control genetic data on lung cancer maintained by the Epidemiology Department at MD Anderson Cancer Center. To investigate incidence of lung cancer we will use public registry data of the SEER type. For disease progression, early detection and intervention, we will use data from the NCI lung cancer chest X-ray screening studies, and the recent ELCAP CT-scan screening study developed at Weill Medical College of Cornell University. The team assembled for the proposed work includes researchers at Rice University, MD Anderson Cancer Center, Weill Medical College of Cornell University and University of California at San Diego, whose documented expertise spans population studies, modeling of natural history of cancer, impact of screening, Bayesian techniques, genetic epidemiology, statistical genetics and risks analysis of smoking. Data used and generated by the project, as well as software, will be made available to CISNET members. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR ALTERATIONS IN LUNG CARCINOGENESIS Principal Investigator & Institution: Mao, Li; Associate Professor/Director; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 20-AUG-2001; Project End 31-JUL-2006 Summary: (provided by applicant): Early lung tumorigenesis is poorly understood at the molecular level. Consequently, no validated molecular marker is currently available for lung cancer risk assessment or evaluation of therapeutic efficacy. We previously demonstrated that certain genetic alterations commonly found in lung cancers might occur in normal-appearing bronchial epithelium of smokers. Altered expression patterns of tumor suppressor genes/oncogenes could also be detected in the bronchial epithelium of smokers. Recently, we found that DNA methylation status in promoter regions of genes involved in tumorigenesis could be altered, not only in lung tumors but also in the bronchial cells of smokers without cancer, resulting in transcriptional repression or activation of these genes. Recent advances in human genome project and high-throughput technologies provide opportunity to accelerate discovery of biomarkers for cancer risk assessment and evaluation of therapeutic efficacy. We hypothesize that substantial molecular alterations occur in airway of smokers, which causes "field defect" and associates with an increased lung cancer risk in this population. As a result, these molecular alterations critical in the initiation of transformation and early progression may predict lung cancer risk and can be used as intermediate endpoints to assess efficacy of chemopreventive agents. Three specific aims are proposed: (1) To identify molecular alterations in smoking damaged lungs and determine their role in assessing efficacy of chemopreventive agents. We will focus on molecular abnormalities that involve critical pathways and can be frequently detected in the bronchial epithelial cells in smokers. Potential differences between current and former smokers will also be analyzed. (2) To determine the role of easily accessible tissues as surrogate materials in evaluating lung damages and chemopreventive effects in the lung. We will determine molecular alterations in sputum and oral brushes in smokers and more importantly to see if potential drug effects in these specimens may reflect those in lung bronchial epithelium. (3) To identify novel biomarkers for risk assessment and evaluation of effects of chemoprevention. In this exploratory aim, we will identify proteins abnormally expressed in carcinogen damaged lungs with high risk to develop lung cancer as well as proteins modulated by chemopreventive agents. We believe that the success of this project will significantly improve our understanding of
38 Lung Cancer
early lung carcinogenesis at the molecular level and provide useful molecular markers for lung chemoprevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR CLONING OF A T(15;19) IN LUNG CANCER CELL LINE Principal Investigator & Institution: Dang, Thao P.; Medicine; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: This is an application for a K08 award for Thao Dang, M.D. designed to support five-years of laboratory training to further develop her skills in molecular genetics and to explore a novel mechanism of carcinogenesis. Malignant transformation is the result of an accumulation of genetic abnormalities. Specific chromosomal translocations are a major mechanism for oncogene activation in hematopoietic malignancies, but have not been described in the much more common epithelial tumors. We have established a cell line, HCC2429, from an aggressive, metastatic lung cancer that has a normal karyotype except for a single translocation between chromosomes 15q and 19p. Using positional cloning we demonstrated that the breakpoint on chromosome 19 lies approximately 40 kb upstream from the start site of Notch3, a member of the Notch proto- oncogene family. This translocation is associated with massive overexpression of Notch3, supporting the hypothesis that the t(15;19) translocation results in the deregulation of this putative cellular proto-oncogene. Furthermore, we have also demonstrated Notch3 over-expression in a panel of lung cancer cell lines and shown that it is highly correlated with translocations involving 19p. We have therefore identified a novel recurring mechanism for oncogene activation in lung cancer as well as a putative oncogene not previously known to be involved in human cancer. Under the mentorship of Dr. David Carbone, Dr. Dang will complete the molecular characterization of the identified t(15;19) translocation, determine the spectrum of the Notch3 receptor and ligand expression in lung cancer and normal tissues, and perform studies to characterize the transforming nature of Notch3 and its effects on downstream signaling pathways in lung cancer. The research environment at the Vanderbilt Ingram Cancer Center is of exceptional caliber and will provide Dr. Dang with the opportunity to interact with experienced molecular biologists as well as geneticists. The support given by this K08 award will allow Dr. Dang to build on her existing knowledge and promote her transition to an independent investigator in a highly competitive environment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR EPIDEMIOLOGY OF SECONDARY LUNG CANCER Principal Investigator & Institution: Shields, Peter G.; Professor & Chief; V T Lombardi Cancer Res Center; Georgetown University Washington, Dc 20057 Timing: Fiscal Year 2003; Project Start 15-JAN-2003; Project End 31-DEC-2007 Summary: (provided by applicant): Several studies indicate that women with breast cancer who undergo radiotherapy are susceptible to secondary lung cancer, whether they are smokers or nonsmokers. However, all studies to date have methodological limitations and have been small. Also, none have used molecular markers, which can improve exposure assessments or elucidate mediating mechanisms. Over time, radiotherapy methods have changed and doses to the lung have lessened. On the other hand, prevalence of smoking has increased among women in the western world. The
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identification of lung cancer risk is important in the context of the debates for benefits of radiation therapy in good prognosis tumors or older women. Thus, a study of breast and secondary lung cancer is needed to improve dosimetry assessments for radiation induced lung cancer, with and without an interactive effect of smoking. Also, studying a unique population of women who have had both breast and lung cancer can provide new insights into carcinogeneis and cancer risk. In order to do this, we are proposing a population-based study using the Swedish Cancer Registry (SCR) and determination of radiation doses to the whole lung and side of the lung where the tumor subsequently develops. Reliable smoking data will be available. Our specific aims are to: 1) determine risk factors for secondary lung cancer in women treated with radiotherapy for breast cancer using complementary nested case-control and case-only study designs (n=559 cases and 559 matched controls); 2) to determine p53 inactivation pathways, (i.e., mutational spectra and loss of heterozygosity) in lung tumors of women with a prior history of breast cancer (n=402) and; 3) to determine the frequency of p53 inactivation pathways in breast tumors of women who did and did not develop lung cancer, and compare them to the frequency of p53 inactivation pathways in the lung tumors (n=342 cases and 342 controls). The first aim will allow us to identify risks. The second aim will provide information about the mechanistic relationship of radiotherapy to lung cancer and may identify a unique spectrum for radiation-related lung cancer. The third aim considers the combined occurrence of breast and lung cancer in a woman as phenotype of susceptibility for multiple primary cases. This study provides unique opportunities. Using the SCR and the unparalleled ability to obtain tissue blocks dating back to the 1950's, we can provide new data to understand risk in the context of molecular markers, especially because we will be able to retrieve the tumor blocks from both the breast and lung cancer from the same women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR STAGING AND SCREENING OF LUNG CANCER Principal Investigator & Institution: Ahrendt, Steven A.; Surgery; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2001; Project Start 01-MAR-1998; Project End 31-MAY-2003 Summary: (Applicant's Description): Lung cancer is the leading cause of cancer related deaths among both males and females in the United States. Surgical resection remains the only curative therapy for patients with non-small cell lung cancer (NSCLC). Despite undergoing curative resection, a large percentage of patients (30 to 40%) with stage I (node-negative) NSCLC develop recurrent disease. Improvements in adjuvant therapy and in the ability to identify those patients most likely to benefit from adjuvant therapy are essential to improving survival in patients with NSCLC. The proposed study uses common molecular genetic events in the neoplastic progression of NSCLC to improve the ability to assign pathological stage, determine prognosis, and to detect disease recurrence in patients with early stage disease. The influence of p53 and K-ras gene mutations on disease-free and overall survival will be examined in patients with nodenegative NSCLC. Molecular techniques will be used to determine the presence of micrometastatic disease in regional lymph nodes in patients undergoing surgical resection. The influence of micrometastatic disease on clinical outcome will be determined for patients with stage I NSCLC. In addition, tumor-specific p53 and K-ras gene mutations and/or microsatellite alterations will be identified in the serum DNA of patients with early-stage NSCLC and their presence correlated with clinical outcome. Completion of the research project will enable the candidate, an Assistant Professor in General Surgery with a strong interest in surgical oncology, to learn state-of-the-art
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molecular techniques with previously demonstrated clinical utility in the staging and screening of patients with cancer. The mentor's laboratory is an ideal place to pursue this project having made substantial contributions in this field. In addition, the wider network of investigators in the field of cancer genetics at the candidate's institution provides a constructive setting for critical review and support of ongoing research in this field. Completion of the proposed mentored training period will provide the candidate with an excellent foundation for pursuing his long-term goals in academic surgical oncology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOUSE MODELS OF LUNG CANCER Principal Investigator & Institution: Boivin, Gregory P.; Pathology and Lab Medicine; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Dr. Boivins's immediate career objectives are to excel in primary and collaborative research efforts, to start a fellowship program in Mouse Pathology, and a training program in Laboratory Animal Medicine. This proposal will alleviate service work so that the fellowship and training program can be pursued and will provide funding for developing a primary research focus. Training and mentoring of high school students, undergraduates, graduate students, postdoctoral fellows, and faculty members will also continue to be performed in two general categories: unstructured or one-on-one time and structured time spent in courses or classes. Alleviation of service work will allow expansion in these areas. Lung cancer is the most common malignant tumor worldwide and is subsequently the greatest cause of cancerrelated mortality. The identification of genes mutated in lung cancer has pointed to some of the signal transduction abnormalities, such as changes in RAS signaling, that occur in the establishment of these tumors. Additionally, mouse-modeling experiments have shown that transgenic mice over expressing Fgf-7, Fgf-10, or activated K-Ras in lung epithelium exhibit epithelial hyperplasia, adenoma, and carcinoma, respectively. Preliminary data have shown that tumor formation in the mouse can be promoted by altering the genotype of mice at the BIm locus. The experiments proposed here will establish and validate mouse models of lung cancer by manipulating the genetic background of the mouse to increase the expression of tumor-promoting factors by increasing somatic recombination and mutation. Tumors will be characterized genomically and by transcription profiling in order to identify other genes altered in the lung tumor formation. This work will test the hypothesis that haploinsufficiency of BIm will increase tumor progression in transgenic mouse models of lung tumorigenesis by increasing mutation rates. The long term aims are to establish in vivo models of lung neoplasia in the mouse in order to identify and characterize the signaling pathways and genes that are disrupted in the development of these tumors, to use these models to identify early markers of tumor development in the lung, and to identify therapeutic targets for human lung cancer therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MUTATION AND ENVIRONMENTAL EXPOSURES Principal Investigator & Institution: Hunt, Jay D.; Professor; Biochem and Molecular Biology; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2001; Project Start 03-APR-2001; Project End 31-MAR-2004
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Summary: (Provided by Applicant) Elevated mortality rates of lung cancer along the Mississippi River in Louisiana have been documented for 50 years and are among the highest in the nation. The Lower Mississippi River interagency Cancer Study (LMRICS, Elizabeth T. H. Fontham, Dr. P. H., PI) is funded by the EPA to conduct a populationbased case-control study of lung cancer in the river parishes. LMRICS will collect tumor samples and exposure data for analysis. The ACS has funded Jay D. Hunt, III, Ph.D. to test the hypothesis that the elevated incidence of lung cancer in the river parishes is associated with chronic exposure to occupational and environmental chemical carcinogens, in addition to tobacco carcinogens, in susceptible individuals as defined by specific phase I and phase II genetic polymorphisms resulting in mutations in key regulatory genes in somatic cells. This funded project will provide the necessary research experience for Dr. Hunt's career development as a molecular epidemiologist. Dr. Elizabeth Fontham will serve as Dr. Hunt's mentor. This application proposes a structured approach to Dr. Hunt obtaining formal training in epidemiology and biostatistics. With this formal training in epidemiology and biostatistics, he will be able to obtain his long-term goals of integrating his training in molecular genetics with molecular epidemiology. Dr. Hunt's long-term career goals are: (1) to continue in his academic, full- time tenure-track position conducting basic and translational molecular genetics studies of non-small cell lung cancer and stomach cancer; (2) to integrate the findings at the bench to develop new biomarkers of prognosis and progression in lung cancer and stomach cancer; and (3) to further develop a molecular epidemiology program in cancer for the Stanley S. Scott Cancer Center at LSUHSC-New Orleans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: NEW STRATEGIES FOR CHEMOPREVENTION OF LUNG CANCER Principal Investigator & Institution: Biswal, Shyam S.; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): This new SPORE project seeks to take promising laboratory leads for lung cancer prevention, beginning with animal models, to proof of principle clinical studies. Our first efforts will explore electrophiles generated after metabolic activation of chemical carcinogens as well as reactive oxygen species. Both are major causes of malignancy. Cancer chemoprevention by induction of protective phase II proteins to counteract the effects of these carcinogens has gained considerable attention. Isothiocyanates have proved to be potent inducers of phase II proteins and compelling epidemiological evidence suggests that dietary isothiocyanates are linked with decreased incidence of lung cancer. Deciphering the downstream targets of isothiocyanates can help in developing these compounds for cancer chemoprevention. The genes for phase II proteins contain the antioxidant or electrophile response element (ARE), which regulate their basal and/or inducible expression. Nrf2, a member of the basic leucine zipper family plays a central role in activation of these genes by binding to ARE in response to its activation by chemopreventive agents. Our studies have shown that Sulforaphane, a naturally occurring isothiocyanate, acts as a potent activator of Nrf2. In this work, we used a microarray approach to identify Nrf2 targets in intestine, which included enzymes that detoxify a wide spectrum of electrophiles and tobacco specific carcinogens. The strategy of activation of Nrf2 for induction of phase II proteins recently has been shown to be effective among former smokers in a phase II b trial using anethole dithiolethione in lowering progression of pre-existing dysplastic lesions and appearance of new lesions. This proposal will focus on the hypothesis that activation of Nrf2 in lungs by Sulforaphane can lead to protection against lung cancer with the
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ultimate goal of developing this agent for clinical trials. The downstream targets of Nrf2 activation in lungs, identified using a genomics approach, will serve as biomarkers to monitor the efficacy of Sulforaphane for lung cancer chemoprevention in the NNK inducible A/J mouse lung cancer model. A small clinical trial will evaluate the efficacy of broccoli sprout extract, optimized for high amount Sulforaphane, to activate the Nrf2 pathway in individuals at high risk for lung cancer. Success in these studies will justify larger controlled studies in current and former smokers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: NF KAPPA B MEDIATED CHEMORESISTANCE IN HUMAN LUNG CANCER Principal Investigator & Institution: Jones, David R.; Surgery; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2001; Project Start 05-AUG-2000; Project End 31-JUL-2005 Summary: Lung cancer is the most common cause of cancer death in both men and women. Eighty percent of all newly diagnosed lung cancers are non-small cell lung cancers (NSCLC), and over 75 percent present with advanced stage disease. For this reason as well as the predilection for distant recurrence after complete resection, most patients are treated with chemotherapy alone or in combination with other modalities. Unfortunately, the majority of NSCLC are chemoresistant despite treatment regimens with second or third generation of chemotherapeutic agents. Tumor chemoresistance has been attributed to the ability of cells to overcome programmed cell death (apoptosis). Recently, it has been established that chemotherapy upregulates the NFkappaB transcription factor and this is associated with cellular resistance to chemotherapy-induced apoptosis. With this understanding, experiments were performed to determine whether NF-kappaB provided a similar cell survival signal in NSCLC cell lines following the addition of gemcitabine and cisplatin, two genotoxic agents commonly used to treat NSCLC. Preliminary data demonstrates that these chemotherapeutic agent induce NF-kappaB transcriptional activity. More importantly, the loss of NF- kappaB sensitizes NSCLC cell lines to chemotherapy-induced apoptosis. Although cell death induced by chemotherapy involves death receptor pathways in certain cell types, chemotherapy- induced apoptosis in NSCLC cells did not involve either Fas- or caspase-8-dependent death receptor pathways. In contrast, NF- kappaB was required to overcome mitochondrial-mediated apoptosis following chemotherapy addition. In addition, ceramide has recently been shown to inhibit the anti-apoptotic P13K/Akt pathway as well as activate NFkappaB. Since the loss of NF- kappaB activity sensitizes NSCLC cells to chemotherapy-induced apoptosis, the major goal of this proposal is to examine the cell signaling mechanisms governing apoptosis and chemoresistance following the addition of chemotherapy. To achieve this objective, we will use established (by the P.I.) cell lines which lack NF-kappaB activity and compare them to controls. These cells will be exposed to chemotherapeutic agents and apoptotic and anti-apoptotic signaling pathways will be examined in vitro. The specific aims of the proposal are to: 1) establish whether chemotherapy kills NSCLC cells through mitochondrial-dependent mechanisms, 2) determine whether the redox status of the cell is responsible for modulating NF-kappaB-dependent cell survival in response to chemotherapy, and 3) determine the role of ceramide as both a pro- and anti-apoptotic mediator following chemotherapy. These studies will provide important insight into how chemotherapy activates apoptotic pathways, as well as mechanisms by which tumors become chemoresistant through upregulation of NF-kappaB. The ultimate goal
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of this study is to provide the necessary background for the initiation of novel treatment strategies designed to treat patients with advanced lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ONCOGENESIS IN RETROVIRUS-INDUCED LUNG CANCER Principal Investigator & Institution: Palmarini, Massimo; Med Microbiol & Parasitology; University of Georgia 617 Boyd, Gsrc Athens, Ga 306027411 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAY-2006 Summary: (provided by applicant): The object of this proposal is to study the mechanisms of oncogenesis in ovine pulmonary carcinoma (OPC), a naturally occurring lung cancer of sheep. OPC is caused by a retrovirus known as Jaagsiekte sheep retrovirus (JSRV). OPC has strikingly similarities with human bronchioalveolar carcinoma (BAC), a lung tumor that is only weakly associated with cigarette smoking and now represents a quarter of all lung cancers in the U.S. Animal models of retrovirus-induced neoplams have given insight into the genetic basis of cancer and have led to the discovery of oncogenes. Thus, OPC is a unique model to investigate lung carcinogenesis and the only viral-induced pulmonary neoplasm in domestic animals. The causal association between JSRV and OPC has been demonstrated by the isolation of an infectious and pathogenic molecular clone (JSRV2 1) but the mechanisms used by JSRV to induce cell transformation are not known and are the object of this proposal. The expression of the JSRV envelope is sufficient to induce transformation of rodent fibroblasts in classical transformation assays. These results suggest a novel mechanism in retroviral-induced oncogenesis. Preliminary results show that the antiapoptotic cell signaling pathway initiated by phosphoinositide-3 kinase (Pl-3K) is constitutively active in JSRV-transformed NIH3T3 but not in the parental cell line. In addition, replication competent JSRV mutants that have lost the ability to transform rodent fibroblasts in vitro have been obtained. These mutants have a single a single point mutation in a tyrosine of the cytoplasmic tail of the transmembrane region of the JSRV envelope altering a putative docking site for PI-3K. These results create an exciting rationale for this proposal whose aim is to dissect and understand the mechanisms of JSRV-induced carcinogenesis both in vitro and in vivo in its natural host. Aim 1 is to dissect the signal transduction pathway initiated by the JSRV envelope in rodent fibroblasts and in cell lines obtained from naturally occurring OPC tumor. However, the mechanisms of carcinogenesis in vivo are likely to be more complex that those followed by JSRV to transform immortalized cell lines. In Aim 2, newborn lambs will be inoculated with JSRV-based vectors and mutants that will determine whether the expression of the viral envelope and the activation of the PI-3K signaling cascade are necessary and/or sufficient to induce lung carcinogenesis. Aim 3 is to look for further mechanisms contributing to oncogenesis in OPC by analyzing the viral insertion sites in naturally occurring OPC-cases. The completion of these experiments will clarify the molecular mechanisms of JSRV-induced pulmonary carcinogenesis and might furnish an intellectual framework to unravel the pathogenesis of some forms of human lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHARMACODYNAMIC PHASE II BREAST, LUNG AND OVARY TRIALS Principal Investigator & Institution: Doroshow, James H.; Associate Director for Clinical Research; City of Hope National Medical Center Duarte, Ca 91010
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Timing: Fiscal Year 2001; Project Start 30-JUN-1994; Project End 31-JUL-2001 Summary: The objective of this proposal is to develop novel, laboratory-based chemotherapeutic treatment strategies for patients with cancers of the breast, lung, and ovary. This goal will be pursued through the formation of a consortium of molecular pharmacologists and clinical investigators from two NCI-designated Cancer Centers and a large University Hospital who will utilize the extensive patient resources of the City of Hope National Medical Center (COH), the Kenneth Norris, Jr. Comprehensive Cancer Center at the University of Southern California (USC), and the University of California, Davis Cancer Center (UCD) to perform pharmacologically-guided Phase II clinical trials that focus on: a) novel high-dose chemotherapies with peripheral blood progenitor cell reinfusion, the molecular pharmacodynamics of the folatefluoropyrimidine interaction, and combination anthracycline resistance modulation studies for patients with advanced breast cancer; b) modification of intrinsic platinum resistance, chemotherapy dose intensification, new agent development, and clinical radiation sensitization for individuals suffering from small cell and non- small cell lung cancer; and c) targeted intraperitoneal and high-dose chemotherapy investigations for women with cancer of the ovary. This application formalizes an ongoing series of collaborative interactions among these three institutions that have existed since the mid1980's. Based on the availability of over 6,250 new cancer patients per year (including 710 with breast cancer, 594 with lung cancer, and 157 with ovarian cancer in 1991), and on the major strengths of the consortium in the areas of bone marrow transplantation, the clinical pharmacodynamics of the fluoropyrimidines and the antifols, as well as pioneering experience in the quantitation of relative gene expression from small amounts of human tumor tissue, the biochemical pharmacology of the anthracyclines and platinum compounds, and clinical research strengths in regional chemotherapy, the development of novel treatment regimens, and biostatistics and data management, the COH-USC-UCD Phase II Consortium is well-positioned to utilize its clinical research expertise to perform complex, laboratory-supported investigations of both new agents and new strategies to enhance therapeutic outcomes for patients with cancers of the breast, lung, and ovary. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PHASE I/II TRIAL OF ZD1839 AND CELECOXIB IN EX-SMOKERS Principal Investigator & Institution: Kelley, Michael J.; Associate Professor of Medicine; Medicine; Duke University Durham, Nc 27706 Timing: Fiscal Year 2002; Project Start 26-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Cigarette smoking is causally associated with development of cancer of the lung, head & neck region, esophagus, bladder, and other sites by overwhelming epidemiological and biologic evidence. Cessation of smoking results in a slow decline in risk of cancer development that remains elevated compared to never smokers beyond 15 years after smoking cessation. Thus, strategies to reduce the impact of lung cancer in former smokers are needed. The epidermal growth factor receptor (EGFR) and cyclo-oxygenase II (COX-2) have been implicated in the development and maintenance of lung cancer. Clinical trials of the EGFR tyrosine kinase inhibitor, ZD1839, in patients with established cancer have demonstrated biological and anti-tumor effects. In the first part of this application, a Phase I, openlabel, dose escalation clinical trial will be conducted to determine the maximal tolerable dose of ZD1839, and the associated effect on EGFR signaling, when used as a chemopreventive agent in former smokers. Former smokers treated with curative intent for early stage lung or head and neck cancer will be treated in cohorts of escalating
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doses of ZD1839. Measures of drug effect (EGFR, c-fos, apoptosis) and biomarkers of lung cancer risk will be measured in bronchial epithelium before and after taking drug for 12 weeks. Potential efficacy of EGFR and/or COX-2 inhibition (using ZD1839 and Celecoxib, respectively) will then be assessed in a Phase II, placebo-controlled, clinical trial assessing effect on bronchial epithelial genetic loss and other surrogate biomarkers of lung cancer risk. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PILOT -- PSYCHOLOGICAL SUPPORT BY TELEPHONE: PILOT OF A NOVEL PSYCHOTHERAPY Principal Investigator & Institution: Holland, James F.; Professor and Chairman; SloanKettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: Presently in the US, 58% of people diagnosed with cancer are 65 years or older (163). Illness is an added burden to other existing or anticipated losses: loss of spouse, friends, family, loss of hearing, sight, and mobility, and reduced independence all further compromise the ability to cope with cancer and its treatment. Colon and lung cancer are more often seen in older age. In fact, 76% of people who have colon cancer and the majority of those who have lung cancer are 65 years or older (163). Lung cancer patients have the highest distress levels (43.5%), and those with colon cancer, 31.6% (162). However, many elderly patients who are severely distressed go unrecognized in the busy clinics and their distress remains undiagnosed and untreated. (165-168). Additionally, it is often difficult for patients with advanced stages of cancer to receive psychological treatment due to physical limitations and inability to come to outpatient clinics. A pilot of a study of telephone counseling for older patients is proposed to provide psychological support. It will examine the delivery over the telephone of a newly developed integrative psychotherapy with patients age 65 and older who have diagnoses of stage IV colon or stage IIIB/IV lung cancer. The psychotherapeutic model is an integrative intervention influenced by the work of Folkman (169). She found that people facing life-threatening events often coped better by finding a tolerable meaning to the event (167). Patients who complete informed consent will receive a telephone counseling intervention that includes 10 counseling sessions across approximately 10 weeks. A pre-and post-assessment will be administered before and following the intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RADIATION THERAPY ONCOLOGY GROUP Principal Investigator & Institution: Curran, Walter J.; Clinical Director, Kimmel Cancer Center; American College of Radiology 1101 Market St, 14Th Fl Philadelphia, Pa 19107 Timing: Fiscal Year 2001; Project Start 01-FEB-1979; Project End 31-DEC-2001 Summary: The Radiation Therapy Oncology Group (RTOG) is an instrument of cooperative investigations to increase survival, decrease morbidity, preserve function and quality of life, and increase basic understanding of cancer. Its clinical, laboratory, and biostatistical scientists have made progress against major killers of Americans, especially cancer of the esophagus, lung, cervix, prostate, and anal canal. It has demonstrated equivalent outcomes when treatments are comparable for blacks and whites with brain tumors, and carcinomas of the head and neck, lung and esophagus, and similar results for women and men with malignant gliomas, head and neck and lung cancer. The RTOG plans to continue integration of surgical, radiotherapeutic and
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chemotherapeutic treatments with emphasis on enhancing local-regional tumor control to improve outcomes. It will continue to investigate 3-dimensional conformal radiation therapy and stereotactic radiosurgery, altered fractionation, and chemical and biologic agents. Phase III trials for brain, head and neck, lung, gastrointestinal and genitourinary tumors are active and new hypotheses will be tested within the RTOG or the integroup mechanism when current studies are completed. A comprehensive quality management program monitors protocol compliance, completeness and accuracy of data, institutional audits and timely reporting of results. The RTOG has an entirely independent data safety and monitoring committee, and its protocols are overseen by an institutional review board with expertise in medical ethics. A Translational Research Program (TRP) chaired by a new Vice-Chair for Basic Science is rapidly advancing correlative studies of clinical, cellular and molecular phenomena; the TRP includes pathologists, tumor biologists and physicians representing all disease sites. A new Vice-Chair for Cancer Control oversees interrelated Community Clinical Oncology Program (CCOP), Special Populations, Epidemiology, Late Effects and Quality of Life investigations. The large databases and long-term observations from RTOG studies serve as unique resources to study major types of cancer. A 19% increase in annual accrual of patients for the last three years compared with the prior four years indicates that the studies of the RTOG investigations will be achieved more rapidly and its results will be available to the practice community and to investigators developing future studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: RADIODIAGNOSIS & RADIOTHERAPY OF LUNG CANCER METASTASES Principal Investigator & Institution: Kassis, Amin I.; Professor/Director; Radiology; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-JAN-2001; Project End 31-DEC-2004 Summary: Lung cancer claims approximately 150,000 lives each year in the USA and its incidence is increasing globally. Early diagnosis of this disease is difficult to obtain. The five-year survival rate of patients with lung cancer is approximately 14 percent and has not changed over the past several decades. The purpose of the proposed research is to establish the potential of the thymidine analog 5-iodo-2'-deoxyuridine (IUdR) radiolabeled with the gamma-emitting isotope iodine-123 (I-123) for the scintigraphic detection of lung cancer and radiolabeled with either the Auger electron-emitting isotope iodine-125 or the beta-emitting isotope iodine-131 for the therapy of lung cancer. To this end, experiments have been designed to examine the specific uptake of radiolabeled IUdR in nude mice bearing cancer cells growing within the lungs. The approaches described should provide an opportunity for the selective targeting of dividing cancerous cells within the lungs and lead to methods for scintigraphic detection of lung cancer as well as development of an effective/adjuvant therapeutic approach. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RAS/RAF/RHO DIFFERENTIATION
IN
LUNG
CANCER
GROWTH
AND
Principal Investigator & Institution: Nelkin, Barry D.; Associate Professor; Oncology Center; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2006
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Summary: (provided by applicant) This project will continue our long term interest in investigating the mechanisms of control of lung cancer cell behavior, focusing on ras/raf-mediated signal transduction pathways. We have shown that raf activation can induce growth arrest in small cell lung cancer (SCLC), but not in non small cell lung cancer (NSCLC), This growth arrest is accompanied by induction of cyclin dependent kinase inhibitor expression; in at least some cell lines, p27Kip1 is induced by translational control. We hypothesize!) that raf activation may mediate growth arrest via translational control in SCLC cells, 2) that this growth arrest can be blocked by activation of rho family protein signal transduction, which may be more active in NSCLC than in SCLC cells, and 3) raf effects on SCLC cells may be mediated in part by autocrine or paracrine mechanisms. The level of activation of the rho family signal transduction pathway will be examined in SCLC and NSCLC cells. In a complementary series of studies, the effect of activating or inhibiting rho family signal transduction in SCLC cells will be investigated, focusing on the effects of rho family members on rafmediated growth arrest. The mechanism of induction of p27kip1 by translational activation during raf-mediated growth arrest in SCLC cells will be investigated. The role of the translation initiation factor eIF4E will be examined. The ability of translational activation to induce cyclin dependent kinase inhibitors and cell cycle arrest in SCLC cells will be determined. The role of autocrine ligands in mediating the effects of raf activation in SCLC cells will be investigated. Identification of two raf-induced autocrine lung cancer derived factors, LCDF I and LCDF2, will be completed. LCDF 1 induces Phosphorylation of MAPK and accumulation of p27, and LCDF2 induces morphological changes in SCLC cells. The ability of LCDF I to promote growth arrest will be determined. The receptor for LCDF 1 will be isolated, and its signal transduction pathways will be identified. The expression patterns for LCDF 1 and its receptor, and LCDF2, will be determined in lung cancer cell lines and primary tumors. The factors responsible for raf-mediated induction of LCDF 1 in SCLC cells will be identified. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: RECEPTOR TYROSINE KINASE INHIBITION AND RADIATION Principal Investigator & Institution: Hallahan, Dennis E.; Professor and Chairman; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): We have identified a novel survival pathway within tumor vascular endothelium that enhances the therapeutic effects of ionizing radiation. Considering that radiation therapy is the primary modality of treatment for unresectable lung carcinoma, improving the efficacy of this treatment is important to improve the cure rate of lung cancer patients. In this regard, we have collaborated with several pharmaceutical companies that are developing small compounds that inhibit specific enzymes within the tumor endothelium. We will only investigate compounds that have entered or will enter clinical studies within the next 3 years. These compounds include SU5416 and SU6668 (Sugen) and PTK87/2K222584 (Novartis). These compounds inhibit receptor tyrosine kinases and downregulate the survival pathway within the tumor endothelium. These compounds will also enter clinical studies through the clinical core in this lung cancer SPORE application. An example of the success in this endeavor is the clinical protocol investigating SU5416 with radiation in a neoadjuvant lung cancer study. We anticipate additional studies with other compounds and future phase III trials. In addition to this translational approach, we will also investigate the mechanisms by which Flk-1 antagonists enhance the therapeutic effects of radiation. We will study the PI3 kinase and Akt/PKB signal transduction pathways. Our preliminary findings
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indicate that inhibition of this pathway enhances radiation-induced apoptosis in the vascular endothelium. We have entered into a material transfer agreement with ICOS, Inc. ICOS has identified several small compounds that inhibit specific isoforms of PI3 kinase. We will determine which of these compounds is most effective in enhancing the therapeutic effects of radiation in lung cancer models in mice. These compounds will then be developed at ICOS to enhance the pharmacokinetics and minimize toxicity. The same approach will be taken with Akt inhibitors as they are developed. In summary, findings from these preclinical studies will assist us in the design of phase I and feasibility studies in the clinic through the clinical core in this SPORE application. In addition, our close collaboration with pharmaceutical companies will ensure that these compounds move rapidly into clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: REGULATION OF TELOMERASE BY CERAMIDE IN LUNG CANCER Principal Investigator & Institution: Ogretmen, Besim; Biochem and Molecular Biology; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant) Lung cancer remains to be the leading cause of cancer related deaths in the United States with poor prognosis. Telomerase, which is upregulated in about 85 percent of lung cancers and not detected in normal lung tissues, is extremely important in cellular proliferation and tumor development. Telomerase elongates telomeres at the end of chromosomes. Thus, it is believed that the modulation of telomerase activity, and telomere length may be a potential therapeutic modality for the treatment of lung cancers. However, molecular mechanisms involved in the regulation of telomerase and telomere length in human lung cancers are not known. The sphingolipid ceramide is known as a tumor suppressor lipid, which mediates antiproliferative biological responses in human cancer cells. Preliminary results by the PI show that ceramide can regulate telomerase activity, independent of apoptosis or necrosis. Therefore, this proposal focuses on identifying the molecular mechanisms and function of ceramide in the regulation of telomerase activity, and telomere length in human lung cancer cells. Specifically, this proposal aims at: 1) Defining the role of ceramide in the inhibition of telomerase activity in human lung cancer cells. This will be achieved by determining: a) the effects of exogenous C6-ceramide, its biologically inactive analog dihydro-C6-ceramide, and analyzing the effects of overexpression of glucosylceramide synthase, which attenuates ceramide, and b) the effects of increased generation of endogenous ceramide by over-expression of serine palmitoyl transferase, and bacterial sphingomyelinase on telomerase activity in lung cancer cell lines. 2) Determining molecular mechanisms and signaling pathways by which ceramide inhibits telomerase activity in human lung cancer cell lines. This will be done by: a) examining the role of ceramide in the transcription of hTERT (the catalytic subunit of telomerase) via determining its role on the stability of hTERT mRNA, regulation of hTERT promoter activity, and c-Myc protein stability and ubiquitination, and b) determining if ceramide induces the inhibition of telomerase through phosphatase activation, since PP2A which is a downstream target of ceramide has been shown to alter telomerase activity by dephosphorylating hTERT, and 3) Analyzing the mechanisms by which ceramide mediates rapid shortening of telomere length. This will be done by a) analyzing the effects of ceramide on telomere length, b) examining the role of ceramide on the activity of recently identified telomere end-binding proteins, TEF-42 and hPot1, which are potential regulators of telomere length in human lung cancer cells, and c) identification and cloning of TEF-42 protein. The long-term objective of this proposal is to better
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understand the molecular mechanisms of telomerase regulation, which will then help develop novel and mechanism-driven therapeutic strategies for the treatment of human lung cancers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: RELEVANCE OF FISH OIL DERIVED PGE3 TO LUNG CANCER Principal Investigator & Institution: Newman, Robert A.; Chief, Section of Pharmacology; Clinical Investigation; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2005 Summary: (provided by applicant): We hypothesize that the fish oils, EPA and DHA, can serve as effective chemopreventive agents against lung cancer and that this protective effect is mediated by selective alteration of arachidonate metabolism through cyclooxygenase enzymes to favor production of PGE3 rather than PGE2. The beneficial effect of PGE3 (i.e. inhibition of tumor cell proliferation vs stimulation produced by PGE2) is at present a poorly understood phenomenon. The research proposed in this application will help us determine the efficacy of fish oil against human lung cancer and obtain insight into the pharmacodynamic activity of EPA and DHA on normal and malignant lung epithelial cells. The specific aims of this proposed project are as follows: 1. To compare the time and concentration-dependent inhibitory effect of EPA and DHA alone or in combination on growth of human lung tumor cells, including cells expressing high and low levels of COX-2. 2. To determine changes in eicosanoid metabolism in human normal and cancer lung cells resulting from exposure of cells to EPA and DHA. The relative effect of these fish oils will also be examined against purified human recombinant COX-1 or COX-2 enzymes using our new and highly specific LC/MS/MS method that simultaneously and rapidly determines prostaglandins (e.g. PGE2 and PGE3) as well as selected lipoxygenase enzyme products (5-, 8-, 11-, 12-, and 15-HETE as well as specific leukotrienes such as LTB4 and LTB5). 3. To compare the relative effect of PGE2 and PGE3 at physiological and pharmacological concentrations on lung cell proliferation and mobility. 4. To study the relationship of PGE2 and PGE3 on cell proliferation and motility relative to activation of the cAMPPKA signaling pathway through prostanoid receptors in human normal and cancer cells, and 5. To evaluate the relative efficacy of EPA, DHA and fish oil (containing both fatty acids) in prevention of tumor growth and its correlation to alteration of eicosanoid metabolism in a mouse model of human lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RESOURCE AND QOL CONSEQUENCES OF LUNG CANCER SCREENING Principal Investigator & Institution: Byrne, Margaret M.; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 08-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The primary purpose of this proposal is to provide the candidate with the means, mentorship and structure to achieve the following goals. The intermediate goal is to measure the psychological, quality of life and resource effects of screening for lung cancer using low dose spiral computed tomography (CT), as well as factors affecting adherence to follow up recommendations. The long term goal is to become an independent health services researcher focusing on evaluation of cancer screening programs and promotion of individual decision making in cancer screening.
50 Lung Cancer
The candidate will further develop and utilize research skills in psychological measurement and analysis, cancer epidemiology and cancer screening techniques, and assessment of health care resource utilization through medical claims databases. The career development program will incorporate formal course work, tutorials with experts in specific methodological fields, clinical training through preceptorships and the National Cancer Institute Cancer Prevention and Control summer course, conferences and seminars, and research. The major goal of the proposed research is to measure the psychological and resource utilization consequences for individuals participating in a lung cancer screening program, and adherence to follow up recommendations from screening. The clinical benefits of screening lung CT are as yet uncertain. However, screening CT detects abnormalities in approximately 40% of all screened individuals. To evaluate and improve screening lung CT programs, and to promote informed decision making concerning screening, it is essential to determine the non-clinical effects of screening. The proposed research will recruit patients from an NCI-funded SPORE project on the clinical outcomes of screening lung CT (Joel Weissfeld, P.I., Pittsburgh Lung Screening Study). Self-administered surveys of psychological characteristics and medical care use, medical claims data, and data from the PLuSS study will be collected over time. The proposed K07 research will determine 1) the psychological and resource effects of participating in lung cancer screening, 2) how these effects vary with screening results and individual characteristics, and 3) whether individuals adherence to recommended follow up after screening and what factors affect non-adherence. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: RETINOIC ACID RESPONSE IN HUMAN LUNG CANCER Principal Investigator & Institution: Zhang, Xiao-Kun; Associate Professor; Burnham Institute 10901 N Torrey Pines Rd San Diego, Ca 92037 Timing: Fiscal Year 2001; Project Start 01-AUG-1993; Project End 31-JUL-2003 Summary: Lung cancer is the leading cause of cancer death in the United States. Therefore, more effective methods to prevent and treat lung cancer are urgently needed. Epidemiological and animal studies have demonstrated that vitamin A and its natural and synthetic derivatives, retinoids, are promising agents in preventing the development of lung cancer. However, clinical trials have found no preventative effects of vitamin A against lung cancer development, suggesting that retinoid responses may be impaired in lung cancer cells. The effects of retinoids are mainly mediated by two classes of nuclear receptors, the retinoic acid receptors (RARs) and retinoid X receptors (RXRs), both of which are encoded by three distinct genes, alpha, beta, and gamma. In our previous study, we found that retinoid responses are impaired in a majority of lung cancer cells and that loss of RARbeta is primarily responsible for the defect. In addition, we observed that loss of RARbeta can be attributed to abnormal regulation of a RA responsive element (beta RARE) in the RARbeta promoter, due to low levels of COUPTF that is required to maintain retinoid sensitivity and/or elevated levels of orphan receptor nur77 which inhibits RXR and COUP-TF activities through heterodimers. The loss of RARbeta could also be attributed to low binding activity of a pEA3 binding site in the RARbeta promoter. Furthermore, we demonstrated that nur77 can induce lung cancer cell apoptosis depending on its stimulus. In the proposed study, we will first study the anti-cancer effects of RARbeta by identifying its specific DNA binding sequences and interacting proteins as well as genes mediating its growth inhibition and apoptosis inducing effects. We will then analyze and clone protein that actively binds to pEA3 site and regulates RARbeta promoter activity. In addition, we will study the mechanism by which COUP-TF sensitizes RAREs and their responsiveness to trans-RA.
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Finally, we will investigate how phosphorylation of nur77 regulates its DNA binding and heterodimerization specificity and their involvement in determining the effects of nur77 on trans-RA resistance and induction of apoptosis, and identify genes responsible for its apoptosis inducing effects. Results from these studies will contribute to our understanding of the mechanism by which RARbeta exerts its anti-cancer activities and how the activities are lost in lung cancer cells, and may provide means to increase retinoid sensitivity in lung cancer cells, thereby enhancing the anti-cancer efficacy and spectrum of retinoids against this diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: RISK POLYMORPHISMS
MODELS:ENVIRONMENT
VERSUS
METABOLIC
Principal Investigator & Institution: Etzel, Carol; Epidemiology; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): My career goal is to become an established researcher in molecular epidemiology with expertise in genetic epidemiology of cancer. This goal builds upon my previous training in statistical science and statistical genetics, but requires further training in molecular techniques and epidemiology. At the end of this training period, I will be an established researcher in cancer prevention. I have developed a comprehensive education and reentering plan. My education plan will provide intensive instruction in the areas of genetics, cancer biology and epidemiotogic methodologies. I have chosen three mentors who will supervise specific portions of my training. Dr. Xifeng Wu will mentor me in molecular epidemiology; Dr. Christopher Amos will supervise the development and application of the statistical methods; and Dr. Margaret Spitz will provide guidance in cancer epidemiology and cancer prevention and control methodologies. My research proposal will focus on developing risk models for lung cancer. I propose to capitalize on the availability of epidemiologic and genetic marker data from an ongoing case-control study (R01 CA55679) under the direction of Dr. Margaret Spitz. This study currently includes over 2700, mostly Caucasian, lung cancer cases and controls, matched on sex, age, ethnicity and smoking status. I will also utilize data from her completed study involving an additional 597 Mexican- and African-American lung cases and controls. My research goal is to construct robust risk models to characterize the most important genetic and environmental risk factors for lung cancer. I aim to investigate lung cancer risk by simultaneously analyzing genetic and epidemiologic data. The specific aims are: 1. To investigate the effect of missing genotypic data on risk modeling and apply methodology to deal with missing data in the assessment of risk for cancer. This is a real deficiency in many studies and I will investigate approaches to handle missing data. I propose a simulation study to investigate the validity of imputation methods in a case/control framework. As a result of this simulation study I will be able to identify the pros and cons of imputation of missing genetic data. Only after an optimal method to impute missing marker values has been identified will I implement imputation in the lung study data. 2. To build a risk model that simultaneously includes available susceptibility markers and epidemiologic data, including gene-environment and gene-gene interactions. I will employ the methods of multiple logistic regression and CART to model lung cancer as a function of genetic and epidemiologic variables, I will incorporate gene-environment and gene-gene interactions cited in the risk assessment literature as welt as those identified from CART into the risk model, I will explore techniques to compare the models obtained by these two methods in order to arrive at an optimal risk model.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ROLE OF COX2 IN LUNG CANCER ANGIOGENESIS AND METASTASIS Principal Investigator & Institution: Johnson, David H.; Professor of Medical and Surgical Oncolo; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant): Upregulation of cyclooxygenase-2 (COX-2) has been shown to be an early event in colon carcinogenesis. Multiple lines of evidence suggest that COX-2 upregulation is also an early event in the development of non-small cell lung cancer (NSCLC). In humans, COX-2 expression is upregulated in about one-third of atypical adenomatous hyperplasias and carcinoma in situ specimens obtained from lung, and in 70 percent-90 percent of invasive adenocarcinomas of the lung. The proportion of adenocarcinoma cells with increased COX-2 expression is much greater in lymph node metastases than in the corresponding primary tumors. Preclinical data indicate tumors with upregulation of COX-2 synthesize high levels of prostaglandin E2 (PGE2). High PGE2 levels are associated with increased production of proangiogenic factors and enhanced metastatic potential. These findings suggest that an increase in COX-2 expression may play a significant role in the development and growth of NSCLC and possibly with the acquisition of an invasive and metastatic phenotype. Specific inhibitors of COX-2 are now available and may prove useful in understanding the role of eicosanoids in lung cancer pathogenesis as well as in the management of established malignancies and possibly as chemopreventive agents. However, there are limited data on the function of tumor overexpression of COX-2 in lung cancer patients, and no data on whether selective inhibitors actually affect COX-2 activity within the targeted tumor in vivo. We propose to study the effects of specific inhibitors of COX-2 on COX-2 expression, serum VEGF levels and urinary metabolites of PGE2 in patients with lung cancer. Our results will serve as a prelude to clinical trials in which these agents are employed therapeutically. Our preliminary data suggest inhibitors of COX-2 rapidly reduce enzyme activity as determined by measurements of urinary metabolites of prostaglandin and assessment of enzyme activity within the tumor itself. These experiments will expand upon these preliminary results. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF PROTEIN KINASE C IN LUNG CANCER Principal Investigator & Institution: Xiao, Lei; Shands Cancer Center; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: The overall objectives of the current proposal are to investigate the cell typespecific regulatory mechanisms that control the expression of protein kinase C-epsilon (PKC-epsilon) in human lung cancer cells and to define what role the phenotypespecific expression of PKC-epsilon may play in the control of cell growth, transformation, and cellular response to drug treatment. Specifically, the proposed studies are designed to extend preliminary results which indicate that induction of PKCepsilon expression may, in part, contribute to development of a drug resistant phenotype during tumor progression of small cell lung cancer (SCLC). A strategy of direct targeting PKC-epsilon expression using antisense technology as well as expression of wild type and mutant forms of PKC-epsilon will be used. A striking differential expression profile of PKC-epsilon but not other PKC isoforms, is found in
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human lung cancer cell lines. PKC-epsilon is expressed in all of the non-SCLC cell lines tested, but none of the SCLC cell lines. Further, its expression is induced when H82 human SCLC cell line is transformed to a non- SCLC phenotype. This transformation is accompanied with changes in drug sensitivity. Therefore, the molecular mechanisms underlying phenotype-specific expression of the PKC-epsilon isoform will be investigated in detail. The information obtained from the proposed studies should provide a better understanding of the biology of lung cancer at the molecular level. More importantly, the results may provide insight into the molecular basis of developing drug resistance, which may lead to novel antineoplastic strategies. Finally, it is expected that a more precise understanding of the regulatory mechanism of PKCepsilon gene expression will help in the basic understanding of the role(s) PKC may play in human tumor cell proliferation, and how specific interference with PKCmediated signaling pathways may be therapeutically exploited in the treatment of human cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SELENIUM AND LUNG CANCER RISK IN ASBESTOS WORKERS Principal Investigator & Institution: Gottschall, Eva B.; National Jewish Medical & Res Ctr and Research Center Denver, Co 80206 Timing: Fiscal Year 2001; Project Start 21-AUG-2000; Project End 31-JUL-2005 Summary: (Applicant's Description) Lung cancer accounts for more cancer deaths in the United States than breast, prostate and colorectal cancer combined. Efforts to improve early detection, develop successful screening programs and find effective chemopreventive agents are desirable. Selenium has shown promise as a cancer chemopreventive agent in animal and human studies. A putative mechanism of selenium's anticarcinogenic activity is its integral part in cellular antioxidant systems. Asbestos-exposed workers have a well established increased incidence of lung cancer, and asbestos carcinogenesis is thought to involve activated oxygen species. In a crosssectional study of asbestos-exposed workers, a large number of individuals were found to have moderate sputum atypia (28 percent), a marker of lung cancer risk. The major hypothesis of this proposal is that asbestos-exposed workers treated with oral seleniumrich yeast (200gg/day) will show significant improvement in intermediate end-point biomarkers of lung cancer risk compared to placebo; and furthermore, changes in markers of lung cancer will be accompanied by decreases in markers of oxidative cellular damage. The study design is a randomized, placebo-controlled, double blind trial of asbestos-exposed construction trades workers using high selenium yeast supplementation. Markers of lung cancer risk to be examined include sputum cytologic atypia, endobronchial metaplasia/dysplasia, and nuclear morphometry of sputum and endobronchial biopsy specimens. The mechanism of action of selenium will be investigated using markers of oxidative cellular damage, including 8hydroxydeoxyguanosine (a marker of DNA damage), malondialdehyde (a marker of lipid peroxidation), and 8-iso-prostaglandine F2, (a marker of lipid peroxidation), before and after the intervention. The proposed study will assess whether selenium is effective in reversing premalignant lesions indicative of increased lung cancer risk and elucidate potential mechanisms of action of selenium. As such, this study will provide a critical foundation to further establish selenium as a potential chemopreventive agent for human lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
54 Lung Cancer
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Project Title: SELENIUM PREVENTION OF TOBACCO SMOKE-INDUCED LUNG CANCER Principal Investigator & Institution: Fan, Teresa W.; None; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2006 Summary: (provided by applicant) The long-term objectives of the proposed work are to understand the biochemical mechanism(s) of supranutritional Se in chemoprevention and to utilize this information for mechanistic clinical studies. A chemopreventive role of selenium (Se) in cancers has been implicated in several clinical and numerous animal studies but whether Se is effective against tobacco smoke (TS)-induced lung cancers is unknown. Nor is it clear in general on the form(s) of Se that are chemopreventive. Lung cancer is a leading cause of cancer death and TS-induced lung cancer may be on the rise worldwide due to growing smoking habit. Thus, the specific aims of this proposal are: 1) To examine whether dietary Se supplement in the form of selenized yeast (Se-yeast) or its major component selenomethionine (Se-Met) is chemopreventive for mice that have "quit" smoking; 2) To characterize biomarkers of Se action such as apoptotic markers and selenoproteins that have been established in other chemoprevention studies so that Se chemoprevention can be understood better at the molecular level; 3) To investigate whether a synergism exists between Se and other chemopreventive agents such as the glucocorticoid hormone budesonide and retinoid isotretinoin in TS induction of lung cancers. To fulfill these aims, the A/J mice model which is the only animal model for TS-induced lung cancer will be employed. Mice will be pre-exposed to tobacco smoke to induce lung tumors during the recovery phase. The effect of dietary Se-yeast or Se-Met supplement during the recovery phase on tumor incidence and/or multiplicity will be measured to see if Se supplement is effective in reducing tumor formation and if additional Se form(s) in Se-yeast may be active. Major Se metabolites present in Se-yeast in addition to Se-Met will be characterized by a combination of NMR and HPLC coupled to mass spectrometry. The Se action will be characterized both immunocytochemically and in lung extracts by a series of apoptotic markers including cytochrome c release, activation of caspases, production of caspase cleavage products, and DNA fragmentation will be measured, along with the activation of selenoprotein, thioredoxin reductase. These biomarkers are known to be elicited in other Se chemoprevention studies. A similar approach will be used to investigate any interactive effect of Se-yeast supplement and budesonide or isotretinoin administered via inhalation; the latter two agents are also known to cause apoptosis. Biomarker characterization should reveal whether synergism is mediated via apoptosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SLC/6CKINE IMMUNOTHERAPY FOR CANCER Principal Investigator & Institution: Sharma, Sherven; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 13-JUN-2002; Project End 31-MAY-2007 Summary: (provided by applicant): Lung cancer is the number one cause of cancer death in the United States. Lung cancers express tumor antigens but are ineffective as antigen presenting cells. We will utilize secondary lymphoid chemokine (SLC) to localize DC at the tumor site where they can function to present an array of antigenic epitopes. This approach to stimulate specific T cell immune responses would not exclude patients on the basis of HLA phenotype or because of lack of expression of a particular tumor antigen. Thus, this therapy would be available to all lung cancer
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patients in the appropriate clinical setting. We hypothesize that SLC therapy will lead to co-localization of dendritic cells (DC) and Th1 cytokine-expressing lymphocytes. We anticipate that DC will traffick to the tumor site where they will be positioned to process and present autologous tumor antigen (Ag) thus providing access to the entire repertoire of available antigens in situ, both increasing the likelihood of a response and reducing the potential for phenotypic modulation. The overall goal of this proposal is to use murine models to determine the mechanisms of SLC-mediated restoration of antitumor immune responses. Utilizing transplantable murine lung cancer models, different modes of SLC delivery will be evaluated that ultimately may have clinical relevance. The following modes of intratumoral SLC delivery will be assessed: 1) injection of recombinant SLC, 2) injection of irradiated SLC transduced tumor cells, and 3) injection of adenovirus vector expressing SLC. A spontaneous murine lung cancer model will be utilized to evaluate the antitumor efficacy of these modes of SLC delivery by intradermal, axillary lymph node region and systemic i.p. injections. Each of these systems will be evaluated because each has potential advantages in the development of immune based therapy for lung cancer. Specific Aims: 1. To identify the mechanisms of anti-tumor responses in secondary lymphoid chemokine (SLC) therapy. (A) The capacity of SLC to enhance the generation of tumor-specific CTL will be investigated. Tumor infiltrating lymphocytes (TIL), splenic T cells and lymph node derived lymphocytes (LNDL) will be evaluated for cytolytic activity and cytokine release against specific and non-specific tumor targets. (B) The importance of cytokines IFN gamma, IL10, GM-CSF, IL-12, MIG and IP10 in SLC- mediated anti-tumor responses will be assessed. 2. To identify the T cell subsets and cytokines important for the memory phenotype following SLC mediated tumor eradication. (A) Mice having rejected their tumors following SLC therapy will be treated with anti-CD3, anti-CD4, anti-CD8 antibodies before rechallenge with 3LL parental tumors, T cell subsets from mice having rejected their tumors following SLC therapy will be transferred to naive mice before challenge with 3LL parental tumors. (B) The importance of cytokines IFN gamma, IL-10, GM-CSF and IL-12 will be assessed in the memory phenotype after SLC mediated tumor eradication. 3. To evaluate the efficacy of different modes and routes of SLC therapy in a spontaneous murine lung cancer model. Dr. Sharma, has the requisite attributes that predict successful academic independence. He is in an excellent scientific environment and will spend 100 percent effort to this endeavor. Work resulting in this environment will prepare Dr. Sharma for a successful independent career in basic cancer research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SPHINGOLIPIDS AND CHEMOTHERAPY-INDUCED APOPTOSIS Principal Investigator & Institution: Hannun, Yusuf A.; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The sphingolipid ceramide, a bioeffector lipid, is known to regulate anti-proliferative responses in various human cell lines. In particular, it has been shown that various anti-cancer agents cause the elevation of endogenous ceramide levels accompanied by apoptotic cell death in human cancer cells. Preliminary results from this program demonstrate that: i) Treatment of A549 human lung adenocarcinoma cells with chemotherapeutic agents results in the formation of endogenous long-chain ceramide via either the de novo pathway or the hydrolysis of sphingomyelin through the action of sphingomyelinase (SMase); ii) Agents that cause ceramide generation via these two distinct pathways have synergistic cytotoxic effects; iii) Downstream targets of ceramides that are generated via the two distinct pathways
56 Lung Cancer
are distinct. These data lead us to the HYPOTHESIS that there are two distinct mechanisms of ceramide formation, namely the de novo pathway and the hydrolysis of sphingomyelin, which function independently and synergistically in mediating apoptosis and growth suppression in human lung cancer cells. As a corollary, we believe that prevention of ceramide clearance should augment chemotherapy action in lung cancer treatment. Therefore, two specific aims are proposed: 1) To determine whether the two distinct mechanisms of ceramide generation act synergistically in mediating apoptotic cell death and/or growth suppression in lung cancer cells. A) Determine which chemotherapeutic agents activate which of the two pathways; B) establish the synergistic effects of anti-cancer agents which activate neutral sphingomyelinase (NSMase) or the de novo pathway, respectively; C) determine the role of ceramide, generated from each pathway, in mediating the action of chemotherapeutic agents by inhibiting each pathway, and D) establish the synergistic effects of activating the two pathways, by overexpression of SMase and serinepalmitoyl transferase (SPT). 2) To identify the mechanisms by which ceramides generated by the two different pathways act synergistically in mediating apoptosis and/or growth suppression. A) Determine the compartmentalization of these pathways, and analyze whether the sub-cellular compartments in which these two pathways are activated are important for their synergistic action; B) test the corollary that clearance of ceramide attenuates the synergistic effects of ceramides in different sub-cellular compartments; and C) determine the down stream targets of ceramides generated via these two pathways. These studies will offer mechanism-based targets for the development of novel cancer therapeutics involving these two distinct ceramide pathways. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SPORE IN LUNG CANCER Principal Investigator & Institution: Carbone, David P.; Professor of Medicine; Medicine; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 28-JUN-2001; Project End 31-DEC-2006 Summary: (provided by applicant) This Lung Cancer SPORE application is a new application submitted by the Vanderbilt-Ingram Cancer Center and its affiliated institutions. In this proposal, we apply the translational research strengths of the Vanderbilt-Ingram Cancer Center toward reducing the incidence, morbidity, and mortality of lung cancer, by focusing on the discovery and validation of molecular targets for prevention and therapy. In project 1 we are studying the role of specific matrix metalloproteinases and targeted inhibitors in the development and behavior of lung cancer. In Project 2 we are applying sophisticated cDNA microarray and protein mass spectrometry techniques to the identification of molecular fingerprints of lung cancer. These fingerprints could ultimately be used to guide patient care or discover novel molecular targets for therapy. Project 3 studies a new potential molecular target, Notch3, that we identified by mapping a balanced chromosome translocation. This also represents a completely new mechanism for gene activation in lung cancer. Receptor tyrosine kinase inhibitors are an exciting new class of molecularly targeted reagents, and in Project 4 we study their effects on downstream signaling pathways and their use in combination with radiation therapy in anti-angiogenic tumor therapy. In projects 5 and 6 we investigate the role cyclooxygenase 2 (COX2) in the therapy (Project 5) and prevention (Project 6) of lung cancer. We have unique facilities for the analysis of COX2 metabolites and intend to study eicosanoid production by human lung cancer tumors in situ, its association with tumor angiogenesis, and its response to treatment with specific inhibitors in vivo. For Project 6 we propose to use two cohorts with previously collected
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pharmacy data to study the impact of long term COX2 inhibitors on the incidence of lung cancer. The first is a retrospective cohort study over 10,000 enrollees of the Tennessee Medicaid Program who were diagnosed with chronic obstructive pulmonary diseases (COPD) during the period of 1980 to 2002. The second is a population-based cohort and nested case-control studies of over 150,000 users of NSAIDs in North Jutland County, Denmark during the period of 1991 to 2002. In order to accomplish these research goals, we propose 4 cores: administrative, tissue, clinical, and biostatistical. The proposed career development and developmental research programs are tightly integrated with established institutional initiatives with documented track records of identifying and funding promising projects and individuals. We will use these established mechanisms to fund lung cancer-targeted career development and research projects. We believe that these projects, cores, and pilot and career development awards could lead to major improvements in the prevention, diagnosis, and treatment of lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SPORE IN LUNG CANCER Principal Investigator & Institution: Baylin, Stephen B.; Professor of Oncology; Oncology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 30-SEP-1992; Project End 31-MAY-2003 Summary: The Johns Hopkins SPORE program for lung cancer, functioning as a major element of the Johns Hopkins Comprehensive Cancer Center, would represent a multidisciplinary and highly collaborative translational research effort to develop new strategies for early detection, prevention and treatment of lung cancer. Included will be an emphasis upon enhancing entry of new investigators into careers in lung cancer research -- and encouragement of novel research approaches through funding of pilot projects. The work scope of the SPORE addresses most of the research imperatives defined at the 1991 Annapolis Lung Cancer Workshop. A major emphasis is devoted to defining, at a molecular level, the earliest steps in lung cancer evolution. The goal is to develop markers which will be tested for efficacy in predicting and/or detecting early lung cancer and which will serve as new tools for guiding prevention and early treatment strategies. Unique tissue acquisition efforts of a Core Tissue Resource will allow isolated fresh and cultured human bronchial epithelium to be studied for timing of genetic (allelic losses, gene mutations) and epigenetic (changes in DNA methylation, neuroendocrine differentiation, signal transduction events, monoclonal antibody recognition) abnormalities in lung cancer progression. The research will include studies of unique patient cohorts for lung cancer risk, including uranium miners and individuals at genetic risk, and studies of unique rodent models for lung cancer induction. Novel treatment strategies for lung cancer, based on molecular targets defined in the laboratory, will be evaluated in focused clinical trials. Included will be molecular biology and biochemical assays to predict and monitor responses. Novel polyamine analogues active, through a newly defined gene induction event, against non-small cell lung cancer (NSCLC) will receive an initial clinical trial. The observation that retinoids can block a tumor progression step for small cell lung cancer cells, in a laboratory model, will be translated into a clinical trial to prevent, or delay, drug resistance for this cancer. In summary, this SPORE program represents an exciting collaborative opportunity for basic and clinical investigators to translate understanding of fundamental biology into new means to prevent, detect and treat lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STRATEGIES
TARGETING
EARLY
CHANGES
FOR
NEW
SCREENING
Principal Investigator & Institution: Sidransky, David; Associate Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Lung cancer is the leading cause of cancer related deaths in males and females in the United States. Surgical resection remains the only curative therapy for patients with non-small cell lung cancer (NSCLC). Identifying highrisk patients likely to develop cancer within a defined period of time is a clinical and biologic challenge for improving survival in patients with NSCLC. This study aims to use the power of molecular biology to develop and test promising new molecular markers for the identification of patients at risk of developing non-small cell lung cancer. Molecular studies have shown that clonal genetic alterations, e.g. 9p21 deletions, are often present in the lung epithelia of smokers and patients with a previous lung malignancy. This study will examine lung epithelium in smokers with a previous history of lung cancer and controls for the presence of specific chromosomal losses using state of the art techniques. New molecular markers will be developed and confirmed by genome wide SNP microarray analysis in normal appearing, preneoplastic, and malignant lung epithelium. The identified genetic markers will be used to test mucosa at risk in a unique population and develop a profile of genetic changes that predict progression to invasive cancer over a defined period of time. Genetic alterations at critical chromosome loci have been shown to be able to predict the progression of oral precursor lesions to invasive cancer. Our studies will pave the way for the development of similar markers in lung cancer and rapid translation into the clinical setting. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TARGETING FATTY ACID SYNTHASE FOR LUNG CANCER TREATMENT Principal Investigator & Institution: Gabrielson, Edward W.; Associate Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 25-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): This project will target the enzyme, fatty acid synthase (FAS), for the treatment of lung cancer. Our preliminary studies have found that the vast majority of non-small cell lung cancers express high levels of this enzyme compared to normal tissues. This increased expression of FAS is significant because inhibition of this enzyme in cancer cells leads to a metabolic imbalance and cellular apoptosis. In a series of in vivo experiments, we found that treatment of orthotopic xenografts of human mesothelioma cells with an agent that inhibits FAS essentially abolished the growth of established tumors. Furthermore, in preliminary experiments, we found a promising anti-tumoral response of lung cancer orthotopic xenografts (in nude rats) treated with an FAS inhibitory compound. Importantly, these treatments did not result in any recognizable damage to normal tissue but did lead to dose-limiting anorexia. The proposed studies will further develop the use of FAS inhibitory therapy for lung cancer treatment. In the first phase of our preclinical studies, we will compare several novel FAS inhibitory agents, using in vivo and in vivo experimental systems, to identify a lead compound with high level of activity against lung cancer cells and tolerable levels of toxicity/anorexia. In the second phase of the preclinical studies, we will optimize dosing protocols for the treatment of lung cancer orthotopic xenografts
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using this compound. This optimization of treatment protocols could be useful for designing treatment protocols to be applied in the clinical setting. The third pre-clinical aim of this project is to examine the effects of the FAS inhibitory compound when used in combination with other agents, such as those currently used to treat lung cancer or being evaluated for treatment of lung cancer. Because the FAS target represents a pathway distinct from those targeted by other compounds, there is a significant potential that such combinations could have synergistic antineoplastic activity, thus allowing reduction of doses of the respective agents. The final aim of this project is to initiate a phase I clinical trial for a compound identified by the preclinical studies to have the best potential for lung cancer treatment. Successful completion of this phase I trial and the preclinical modeling studies will provide a framework for further evaluation of an FAS inhibitory compound in the treatment of lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: THE BIOLOGY FLUOROTHYMIDINE PET
OF
LUNG
CANCER--
FDG
AND
Principal Investigator & Institution: Vesselle, Hubert J.; Assistant Professor; Radiology; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 12-JAN-2000; Project End 31-DEC-2004 Summary: The objective of the proposed studies is to investigate quantitative [F18]fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) as a measure of non-small cell lung cancer (NSCLC) aggressiveness in vivo (i.e. grading) and to make comparisons with patients' outcomes and with specimen-derived measures of cellular proliferation previously shown to predict poor outcome (S-phase fraction, Ki-67 index). We postulate that, in clinically resectable NSCLC patients, pre-operative FDG PET will show that tumors with higher FDG uptake: (a) will recur sooner after surgical resection than same stage tumors with low uptake; (b) are more likely to have mediastinal or distal metastatic disease than tumors of the same clinical stage but low uptake; (c) have higher S-phase fraction of Ki-67 scores in their resected specimen. The specific aims of the proposal are: (1) Perform whole-body pre- operative FDG PET imaging and correlate FDG uptake in primary NSCLC with outcome. FDG uptake will be quantified by the following methods that will be compared. Standardized Uptake Value (SUV) and SKMFDGMR (FDG Metabolic Rate determined by a Simplified Kinetic Method). (2) Perform whole-body pre-operative FDG PET imaging and correlate FDG uptake (quantified as SUV and SKM-FDGMR) in primary NSCLC with disease extent as demonstrated by PET and surgical staging. (3) Correlate pre-operative FDG uptake in primary NSCLC with markers of cellular proliferation measured from the resected specimen and previously shown to predict poor outcome. Outcome will be measured by recurrence-free survival, time-to recurrence and survival. In summary, by studying NSCLC patients preoperatively, prior to any form of chemotherapy or radiotherapy, we will gain valuable information about the biology of lung cancer, the leading cause of cancer death in the United States. By performing a biologic grading of resectable NSCLC with FDG PET, we will predict which patients will have a worse outcome. This information will allow individualized therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TRANSCRIPTION DEVELOPMENT
FACTOR
NFKB
IN
LUNG
CANCER
Principal Investigator & Institution: Aggarwal, Bharat B.; Professor of Medicine; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030
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Timing: Fiscal Year 2001; Project Start 20-AUG-2001; Project End 31-JUL-2006 Summary: (provided by applicant): Cigarette smoke (CS) causes approximately 80-90 percent of lung cancer in the United States, but the mechanism by which CS mediates its effects is not fully understood. One factor may be transcription factor NF-kB, which regulates the expression of various genes involved in tumor initiation, promotion, and metastasis. We hypothesize that NF-kB activation by CS is an important factor in lung cancer development, and that inhibition of NF-kB activation or the activity of NF-kB regulated gene products (such as cyclooxygenase-2) could prevent lung cancer development. To test this hypothesis, we propose the following specific aims: Specific Aim 1: Determine if NF-kB is activated in biopsies containing bronchial epithelial cells from former and current cigarette smokers before and after celecoxib treatment. Specific Aim 2: Determine if cigarette smoke activates NF-kB and induces the NF-kB dependent gene expression in selected normal, premalignant and malignant lung cancer cell lines. Specific Aim 3: Determine if the cigarette smoke-induced NF-kB activation blocks apoptosis. Specific Aim 4: Determine if celecoxib downregulates cigarette smokeinduced NF-kB activation and overcomes cigarette smoke-induced resistance to apoptosis. Through these studies, we will determine: 1) whether cigarette smoking in humans leads to NF-kB activation and if it is modulated by celecoxib; 2) whether cigarette smoke activates NF-kB and induces NF-kB-dependent gene expression in bronchial epithelial lung cells; 3) whether CS-induced NF-kB results in suppression of apoptosis; and, 4) whether celecoxib can induce apoptosis through suppression of CSinduced NF-kB activation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TUMOR SUSCEPTIBILITY /GENETIC MUTATION /LUNG CANCER RISK Principal Investigator & Institution: Zhang, Zuo-Feng; Director/Professor; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-DEC-2005 Summary: This proposal is built upon an ongoing population-based case-control study on marijuana use and the risk of lung and UAT cancers funded by NIH. The objectives are to better understand the molecular mechanisms for the risk of lung cancer. We propose that the development of lung cancer is an interactive process involving previous environmental exposures such as active and passive tobacco smoking, marijuana smoking; intrinsic host susceptibility such as polymorphisms and methylations of the GST P1 and polymorphisms of the TP53 gene and genetic instability including TP53 and mutations and p16 methylations an and other alterations. The study will be based on 600 cases and 600 controls interviewed by the parent study. Among those, we project 420 lung cancer patients with have their tumor tissue available for the analysis and 488 case and 488 controls will have their buccal cell samples for this proposed study, according to our pilot study. Epidemiological factors will be obtained by face-to-face interview. Our study is designed Our study is designed to fulfill these specific aims. (1) We will assay polymorphisms and hypermethylations of GST P1 in 488 cases and 488 controls, to evaluate will have their buccal cell samples for this proposed study, according to our pilot study. Epidemiological factors will be obtained by face-toface interview. Our study is designed to fulfill these specific aims. (1) We will assay polymorphisms and hypermethylations of GST P1 in 488 cases and 488 controls, to evaluate the effects of those alterations on the risk of lung cancer, and explore geneenvironment interaction between GSTP1 and environmental exposures. Other metabolic genes involved in PAH metabolism such as GSTM1 and P450A1 will be assayed. (2) We
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will measure polymorphisms of TP53 gene in 488 cases and 488 controls and examine the effects of polymorphisms of TP53 gene by a case-control study. We will measure TP53 mutations by PCR-SSCP and sequencing to test the hypothesis that cases with lung cancer with and without p53 mutations are etiologically distinctive groups with regard to major risk factors such as active and passive tobacco smoking, occupational exposure, etc. (3) We will measure p16 methylations and other alterations including mutations, homozygous deletions, and microsatellite instability, and correlate these alterations with tobacco smoking and occupational exposures. The result of this study may provide insight into lung carcinogenesis. It may assist us to identify high-risk individuals for intervention and may have translational potential to screening, early detection and prognostic prediction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: UCLA SPORE IN LUNG CANCER Principal Investigator & Institution: Dubinett, Steven M.; Professor of Medicine; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-DEC-2005 Summary: The UCLA Jonsson Comprehensive Cancer Center has designed a Specialized Program of Research Excellence (SPORE) in lung cancer. This multidisciplinary, translational research program addresses critical questions in a broad based research effort to enhance our understanding of lung cancer biology and develop more effective methods for the prevention diagnosis, and treatment of lung cancer. The UCLA Lung Cancer SPORE is led by experienced lung cancer researchers who have organized investigative teams to develop highly interactive research programs with a strong translational focus. These scientific programs will focus on: 1) Tumor Susceptibility, Genetic Mutations, and Risk of Lung Cancer; 2) A Combined CT-PET Approach to Optimize in vivo Lung Nodule Characterization; 3) Neuropeptide Signaling Antagonists for SCLC Therapy; 4) Genetic Immunotherapy for Lung Cancer; and 5) Chemokine Regulation of Angiogenesis in Lung Cancer. The translational focus of this research will be maintained in each scientific section by teams of both basic and applied investigators. A Developmental Research Program will award 3-5 new grants each years for highly innovative translational research. The selection and progress of these developmental programs will be monitored by the Developmental Programs and Executive Committees, as well as the Internal and External Advisory Boards. A Lung Cancer SPORE Career Development Program designed for both fellows and faculty will be implemented for the career development of translational lung cancer investigators. To promote the strong translational research emphasis we have instituted a Clinical Trials Core that will be responsible for initiating clinical trials that are based on the preclinical investigations in each of the laboratories. Additional cores for pathology, informatics and administration will serve to support all of the research programs within the SPORE. In addition to research based at UCLA, our Lung Cancer SPORE Program is designed to foster collaborative interactions regionally and nationally. Accordingly, we have selected an external advisory board comprised of cancer center directions within our region as well as nationally recognized translational lung cancer researchers. In collaboration with the Lung Cancer SPORE leadership, the Internal and External Advisory Boards will continually assess the progress of all aspects of the program. The UCLA Lung Cancer SPORE is designed for maximum flexibility so that resources can be focused on the most promising investigations with the greatest translational potential.
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The UCLA Lung Cancer SPORE constitutes a highly collaborative, multi-disciplinary translational research program designed to make a significant impact on lung cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: USE OF BETA-LAPACHONE FOR LUNG CANCER CHEMOTHERAPY Principal Investigator & Institution: Boothman, David A.; Professor and Director of Basic Research; Radiation Oncology; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Lung cancer is the leading cause of death by cancer in the U.S. Non-small cell lung cancer (NSCLC) comprises over 75 percent of lung cancers diagnosed. Current chemotherapeutic regimens are not effective against NSCLC, with five-year survival rates hovering at a mere 14 percent. Regimens that exploit cancer-specific targets, specifically in and increase therapeutic indices, should enhance the survival rates of patients. We hypothesize that Beta-lapachone (beta-lap), a drug that selectively kills cancer cells with elevated levels of the two-electron reductase, NAD(P)H:quinone oxidoreductase 1 (NQOI), will be an effective agent for use against NSCLC cells that specifically over-express this bioactivating enzyme. Cell death caused by beta-lap is not dependent on cell cycle status, not dependent on p53, pRb, or caspases, and downstream cell death events are consistent with calpain-mediated apoptosis. More importantly, cell death by beta-lap is dependent on NQO1 expression, where NQO1-deficient cells are resistant to the drug, correction of cells with NQO1 restores lethality, and co-administration of dicumarol (an NQO1 inhibitor) prevents lethality. NQOI is typically elevated 4- to greater than 100-fold in human NSCLC, indicating the use of beta-lap for treatment of this disease. Recent development of novel drug delivery methods make it feasible to administer this drug to determine efficacy against NSCLC in animal models. Three aims will test this hypothesis: Aim 1: Evaluate the role of NQO1 in beta-lap-mediated cell death in NSCLC cells, and develop lab correlates for use in future therapy. (Years 1-3). Aim 2: Develop drug vehicles for betalap that either deliver the drug locally to the lung, or utilize systemic delivery schemes that allow accumulation of the vehicle-drug complexes within the lung, while offering simultaneous treatment for metastatic disease. (Years 1-5). Aim 3: Compare beta-lapencoded microparticles developed in Aim 2 for specific delivery to the lung to systemic delivery (i.p.) of HP-beta-cyclodextrin-beta-lap complexes for NQOl-specific lung tumor responses. We will combine these therapies with systemic dicumarol administration for normal tissue protection. (Years 1-5). We have assembled a strong research team with the needed experience to develop novel drug vehicles, image the deposition and delivery of both beta-lap and the vehicle in the lung, and test the hypothesis that betalap should be an efficacious agent against NSCLC due to tumor-specific elevation of NQO 1, a bioactivating enzyme specifically needed for novel calpain-mediated cell death responses elicited by beta-lapachone. We will examine the possibility that coadministration of dicumarol can act as an antidote, increasing the anti-tumor efficacy of beta-lap. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
·
Project Title: USE OF RADIATION IN STAGE IV NON-SMALL CELL LUNG CANCER Principal Investigator & Institution: Hayman, James A.; Assistant Professor; Radiation Oncology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274
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Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 31-MAR-2004 Summary: (provided by applicant): The primary objective of this project is to examine factors associated with the utilization of radiation therapy in a sample of patients with Stage IV (i.e., metastatic) non-small cell lung cancer diagnosed in selected regions of the U.S. during a period ranging from 1991 to 1996. Anecdotal reports suggest that the use of radiation therapy to palliate symptoms associated with metastatic cancer is common and that there may be substantial variation in the intensity of treatment (i.e., number of treatments). This has important cost and quality implications because studies published over the last decade suggest that shorter courses of radiation treatment may be as effective as longer courses. Although this remains controversial in the U.S., as early as 1994 clinical guidelines in the U.S. began to endorse shorter courses of therapy. We propose to use the population-based linked SEER-Medicare data set to examine patterns and determinants of the utilization of palliative radiation therapy in patients age 65 or greater diagnosed with metastatic non-small cell lung cancer between 1991 and 1996. Created by researchers at the National Cancer Institute, this data set contains clinical data on almost all patients aged 65 and older diagnosed with cancer in the eleven SEER regions that have been linked to their respective Medicare claims data. Specifically, we plan to use SEER data to identify incident cases of metastatic non-small cell lung cancer and then use the Medicare claims data to identify those patients who received radiation therapy and quantify the intensity with which they were treated. We then propose to use this information to identify factors associated with the use and intensity of treatment with radiation including patient predisposing/enabling factors, clinical factors, organizational factors and physician factors. Lastly, we plan to examine whether the frequency and intensity of the administration of treatment with palliative radiation in this patient population has changed over time. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: VIRTUAL TRUE-COLOR BRONCHOSCOPY TO DETECT LUNG CANCER Principal Investigator & Institution: Mclennan, Geoffrey; Associate Professor of Medicine; Internal Medicine; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2005 Summary: (provided by applicant): Lung cancer is the most common cause of cancer death in both men and women in the United States. Reliable generalizable methods to detect early cancer within the bronchoscopically visible (central) airways are urgently needed. This development needs to occur concurrently with other efforts already underway to identify early peripheral lung cancers. The characteristics of early cancer within the human airway are thickening of the airway mucosa, and a change of color of the mucosal surface. At an earlier stage there will likely be protein and molecular changes, but these are so far poorly described. However, the expectation is that within several years there will be fluorescent markers that could be used to identify cancer changes within the human airway at this early stage. Recently there have been major advances in human imaging hardware and software. The first true color CCD bronchoscopes have been commercially introduced within the last 12 months. The digital output provides better color and spatial resolution. CT scanning has also benefited in speed and resolution through the introduction of multislice spiral scanners. One problem with these technologies is that the richness of the digital information further compounds the substantial human observer error rate in reporting on abnormalities. The purpose of this phased innovation award application is to develop digital analytic color detection and analysis of the human airway mucosa with images
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from the CCD color bronchoscope; to develop digital analysis and display of the airway mucosa from high resolution/high speed volumetric CT scan data; and to integrate these two complimentary modalities into a single generalizable early cancer detection tool. At the completion of the project we will have developed this integrated automated and analytic tool, and evaluated this in a human population at high risk for lung cancer. We will be able to define the characteristics of the normal human airway, and the human airway in smoking subjects at high risk of lung cancer. We will know the positive and negative predicted values for airway mucosal lesions determined by CT scan (thickening and abnormal topography), and by abnormal airway color, both separately and collectively against a pathologic gold standard. In the future, we expect this technology to be easily used and generally available for undertaking effective screening for lung cancer within the bronchoscopically visible airways. Such technology will be useful for the evaluation of molecular probes as they are developed, and in promoting image guided airway cancer treatment. Lung cancer is the most common cause of cancer death in both men and women in the United States. Reliable generalizable methods to detect early cancer within the bronchoscopically visible (central) airways are urgently needed. This development needs to occur concurrently with other efforts already underway to identify early peripheral lung cancers. The characteristics of early cancer within the human airway are thickening of the airway mucosa, and a change of color of the mucosal surface. At an earlier stage there will likely be protein and molecular changes, but these are so far poorly described. However, the expectation is that within several years there will be fluorescent markers that could be used to identify cancer changes within the human airway at this early stage. Recently there have been major advances in human imaging hardware and software. The first true color CCD bronchoscopes have been commercially introduced within the last 12 months. The digital output provides better color and spatial resolution. CT scanning has also benefited in speed and resolution through the introduction of multislice spiral scanners. One problem with these technologies is that the richness of the digital information further compounds the substantial human observer error rate in reporting on abnormalities. The purpose of this phased innovation award application is to develop digital analytic color detection and analysis of the human airway mucosa with images from the CCD color bronchoscope; to develop digital analysis and display of the airway mucosa from high resolution/high speed volumetric CT scan data; and to integrate these two complimentary modalities into a single generalizable early cancer detection tool. At the completion of the project we will have developed this integrated automated and analytic tool, and evaluated this in a human population at high risk for lung cancer. We will be able to define the characteristics of the normal human airway, and the human airway in smoking subjects at high risk of lung cancer. We will know the positive and negative predicted values for airway mucosal lesions determined by CT scan (thickening and abnormal topography), and by abnormal airway color, both separately and collectively against a pathologic gold standard. In the future, we expect this technology to be easily used and generally available for undertaking effective screening for lung cancer within the bronchoscopically visible airways. Such technology will be useful for the evaluation of molecular probes as they are developed, and in promoting image guided airway cancer treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “lung cancer” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for lung cancer in the PubMed Central database: ·
3pK, a new mitogen-activated protein kinase-activated protein kinase located in the small cell lung cancer tumor suppressor gene region. by Sithanandam G, Latif F, Duh FM, Bernal R, Smola U, Li H, Kuzmin I, Wixler V, Geil L, Shrestha S.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231067
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A Gene in the Chromosomal Region 3p21 with Greatly Reduced Expression in Lung Cancer is Similar to the Gene for Ubiquitin-Activating Enzyme. by Kok K, Hofstra R, Pilz A, van den Berg A, Terpstra P, Buys CH, Carritt B.; 1993 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46869
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A Vasoactive Intestinal Peptide Antagonist Inhibits Non-Small Cell Lung Cancer Growth. by Moody TW, Zia F, Draoui M, Brenneman DE, Fridkin M, Davidson A, Gozes I.; 1993 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46507
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Aberrant methylation of p16 INK4a is an early event in lung cancer and a potential biomarker for early diagnosis. by Belinsky SA, Nikula KJ, Palmisano WA, Michels R, Saccomanno G, Gabrielson E, Baylin SB, Herman JG.; 1998 Sep 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21736
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Altered HOX and WNT7A expression in human lung cancer. by Calvo R, West J, Franklin W, Erickson P, Bemis L, Li E, Helfrich B, Bunn P, Roche J, Brambilla E, Rosell R, Gemmill RM, Drabkin HA.; 2000 Nov 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18840
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An immune response manifested by the common occurrence of annexins I and II autoantibodies and high circulating levels of IL-6 in lung cancer. by Brichory FM, Misek DE, Yim AM, Krause MC, Giordano TJ, Beer DG, Hanash SM.; 2001 Aug 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=55537
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Antiproliferative and Apoptotic Activities of Ketonucleosides and Keto-C-Glycosides against Non-Small-Cell Lung Cancer Cells with Intrinsic Drug Resistance. by Paterson J, Uriel C, Egron MJ, Herscovici J, Antonakis K, Alaoui-Jamali MA.; 1998 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=105541
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Assessment of whether in-hospital mortality for lobectomy is a useful standard for the quality of lung cancer surgery: retrospective study. by Treasure T, Utley M, Bailey A.; 2003 Jul 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=164918
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Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines by a "biased agonist" mechanism. by Chan D, Gera L, Stewart J, Helfrich B, Verella-Garcia M, Johnson G, Baron A, Yang J, Puck T, Bunn P Jr.; 2002 Apr 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123695
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Conservation of the Drosophila lateral inhibition pathway in human lung cancer: A hairy-related protein (HES-1) directly represses achaete-scute homolog-1 expression. by Chen H, Thiagalingam A, Chopra H, Borges MW, Feder JN, Nelkin BD, Baylin SB, Ball DW.; 1997 May 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24682
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Cyclin D1 Overexpression vs. Retinoblastoma Inactivation: Implications for Growth Control Evasion in Non-Small Cell and Small Cell Lung Cancer. by Schauer IE, Siriwardana S, Langan TA, Sclafani RA.; 1994 Aug 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44495
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Dying of lung cancer or cardiac failure: prospective qualitative interview study of patients and their carers in the community. by Murray SA, Boyd K, Kendall M, Worth A, Benton TF, Clausen H.; 2002 Oct 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130056
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Effects of Renal Function on Pharmacokinetics of Recombinant Human Granulocyte Colony-Stimulating Factor in Lung Cancer Patients. by Fukuda M, Oka M, Ishida Y, Kinoshita H, Terashi K, Fukuda M, Kawabata S, Kinoshita A, Soda H, Kohno S.; 2001 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=90583
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EPA links diesel exhaust, lung cancer. by Weir E.; 2002 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=126532
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Evidence for impaired retinoic acid receptor-thyroid hormone receptor AF-2 cofactor activity in human lung cancer. by Moghal N, Neel BG.; 1995 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230634
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Genomic approaches to research in lung cancer. by Gabrielson E.; 2000; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59540
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Gleevec (STI-571) inhibits lung cancer cell growth (A549) and potentiates the cisplatin effect in vitro. by Zhang P, Gao WY, Turner S, Ducatman BS.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149413
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Hemoptysis as an Unusual Presenting Symptom of Invasion of a Descending Thoracic Aortic Aneurysmal Dissection by Lung Cancer. by Tsui P, Lee JH, MacLennan G, Capdeville M.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116743
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Human lung cancer and p53: The interplay between mutagenesis and selection. by Rodin SN, Rodin AS.; 2000 Oct 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17326
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Human Semaphorins A(V) and IV Reside in the 3p21.3 Small Cell Lung Cancer Deletion Region and Demonstrate Distinct Expression Patterns. by Sekido Y, Bader S, Latif F, Chen J, Duh F, Wei M, Albanesi JP, Lee C, Lerman MI, Minna JD.; 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39497
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Immediate versus delayed palliative thoracic radiotherapy in patients with unresectable locally advanced non-small cell lung cancer and minimal thoracic symptoms: randomised controlled trial. by Falk SJ, Girling DJ, White RJ, Hopwood P, Harvey A, Qian W, Stephens RJ.; 2002 Aug 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=119441
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Increased Cytosine DNA-Methyltransferase Activity is Target-Cell-Specific and an Early Event in Lung Cancer. by Belinsky SA, Nikula KJ, Baylin SB, Issa JJ.; 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39484
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Inhibition of lung cancer cell growth and induction of apoptosis after reexpression of 3p21.3 candidate tumor suppressor gene SEMA3B. by Tomizawa Y, Sekido Y, Kondo M, Gao B, Yokota J, Roche J, Drabkin H, Lerman MI, Gazdar AF, Minna JD.; 2001 Nov 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=61148
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Isolation of DNA Sequences Deleted in Lung Cancer by Genomic Difference Cloning. by Wieland I, Bohm M, Bogatz S.; 1992 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50201
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Jaagsiekte Sheep Retrovirus Is Necessary and Sufficient To Induce a Contagious Lung Cancer in Sheep. by Palmarini M, Sharp JM, de las Heras M, Fan H.; 1999 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112782
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Molecular characteristics of non-small cell lung cancer. by Nacht M, Dracheva T, Gao Y, Fujii T, Chen Y, Player A, Akmaev V, Cook B, Dufault M, Zhang M, Zhang W, Guo M, Curran J, Han S, Sidransky D, Buetow K, Madden SL, Jen J.; 2001 Dec 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65007
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Molecular Determinants of AHPN (CD437)-Induced Growth Arrest and Apoptosis in Human Lung Cancer Cell Lines. by Li Y, Lin B, Agadir A, Liu R, Dawson MI, Reed JC, Fontana JA, Bost F, Hobbs PD, Zheng Y, Chen GQ, Shroot B, Mercola D, Zhang XK.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109058
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Multicentre randomised controlled trial of nursing intervention for breathlessness in patients with lung cancer. by Bredin M, Corner J, Krishnasamy M, Plant H, Bailey C, A'Hern R.; 1999 Apr 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27809
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MYO18B, a candidate tumor suppressor gene at chromosome 22q12.1, deleted, mutated, and methylated in human lung cancer. by Nishioka M, Kohno T, Tani M, Yanaihara N, Tomizawa Y, Otsuka A, Sasaki S, Kobayashi K, Niki T, Maeshima A, Sekido Y, Minna JD, Sone S, Yokota J.; 2002 Sep 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129434
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Nerve growth factor abrogates the tumorigenicity of human small cell lung cancer cell lines. by Missale C, Codignola A, Sigala S, Finardi A, Paez-Pereda M, Sher E, Spano P.; 1998 Apr 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20267
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Neuropeptide Stimulation of Calcium Flux in Human Lung Cancer Cells: Delineation of Alternative Pathways. by Bunn PA Jr, Dienhart DG, Chan D, Puck TT, Tagawa M, Jewett PB, Braunschweiger E.; 1990 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53646
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New transformation tricks from a barnyard retrovirus: Implications for human lung cancer. by Rosenberg N.; 2001 Apr 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33321
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Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. by Minna JD.; 2003 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151841
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Nonconventional Opioid Binding Sites Mediate Growth Inhibitory Effects of Methadone on Human Lung Cancer Cells. by Maneckjee R, Minna JD.; 1992 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48410
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Nurse led follow up and conventional medical follow up in management of patients with lung cancer: randomised trial. by Moore S, Corner J, Haviland J, Wells M, Salmon E, Normand C, Brada M, O'Brien M, Smith I.; 2002 Nov 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=133453
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Opioid and Nicotine Receptors Affect Growth Regulation of Human Lung Cancer Cell Lines. by Maneckjee R, Minna JD.; 1990 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53886
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Plasma PGE-2 levels and altered cytokine profiles in adherent peripheral blood mononuclear cells in non-small cell lung cancer (NSCLC). by Hidalgo GE, Zhong L, Doherty DE, Hirschowitz EA.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149408
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Preferences for chemotherapy in patients with advanced non-small cell lung cancer: descriptive study based on scripted interviews. by Silvestri G, Pritchard R, Welch HG.; 1998 Sep 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28665
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Prophylactic cranial irradiation in small cell lung cancer: a systematic review of the literature with meta-analysis. by Meert AP, Paesmans M, Berghmans T, Martin B, Mascaux C, Vallot F, Verdebout JM, Lafitte JJ, Sculier JP.; 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34096
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Quality of life in lung cancer patients: does socioeconomic status matter? by Montazeri A, Hole DJ, Milroy R, McEwen J, Gillis CR.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165601
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Rapid p53 sequence analysis in primary lung cancer using an oligonucleotide probe array. by Ahrendt SA, Halachmi S, Chow JT, Wu L, Halachmi N, Yang SC, Wehage S, Jen J, Sidransky D.; 1999 Jun 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22094
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Reanalysis of epidemiological evidence on lung cancer and passive smoking. by Copas JB, Shi JQ.; 2000 Feb 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27286
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Recent changes in lung cancer incidence for south Asians: a population based register study. by Smith LK, Peake MD, Botha JL.; 2003 Jan 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=139937
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Reconstituted Basement Membrane (Matrigel) and Laminin can Enhance the Tumorigenicity and the Drug Resistance of Small Cell Lung Cancer Cell Lines. by Fridman R, Giaccone G, Kanemoto T, Martin GR, Gazdar AF, Mulshine JL.; 1990 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54604
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Reduction in receptors for bombesin and epidermal growth factor in xenografts of human small-cell lung cancer after treatment with bombesin antagonist RC-3095. by Halmos G, Schally AV.; 1997 Feb 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19621
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Regular aspirin use and lung cancer risk. by Moysich KB, Menezes RJ, Ronsani A, Swede H, Reid ME, Cummings KM, Falkner KL, Loewen GM, Bepler G.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=138809
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Relation between socioeconomic status and tumour stage in patients with breast, colorectal, ovarian, and lung cancer: results from four national, population based studies. by Brewster DH, Thomson CS, Hole DJ, Black RJ, Stroner PL, Gillis CR.; 2001 Apr 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30560
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Resistance to Taxol in lung cancer cells associated with increased microtubule dynamics. by Goncalves A, Braguer D, Kamath K, Martello L, Briand C, Horwitz S, Wilson L, Jordan MA.; 2001 Sep 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58799
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Serological identification of embryonic neural proteins as highly immunogenic tumor antigens in small cell lung cancer. by Gure AO, Stockert E, Scanlan MJ, Keresztes RS, Jager D, Altorki NK, Old LJ, Chen YT.; 2000 Apr 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18195
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Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies. by Peto R, Darby S, Deo H, Silcocks P, Whitley E, Doll R.; 2000 Aug 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27446
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The exogenous form of Jaagsiekte retrovirus is specifically associated with a contagious lung cancer of sheep. by Palmarini M, Cousens C, Dalziel RG, Bai J, Stedman K, DeMartini JC, Sharp JM.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189985
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Three Tumor-Suppressor Regions on Chromosome 11p Identified by HighResolution Deletion Mapping in Human Non-Small-Cell Lung Cancer. by Bepler G, Garcia-Blanco MA.; 1994 Jun 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44026
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Tumor-Suppressive Effect of the Retinoic Acid Receptor [beta] in Human Epidermoid Lung Cancer Cells. by Houle B, Rochette-Egly C, Bradley WE.; 1993 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45795
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Vasoactive intestinal peptide inhibits human small-cell lung cancer proliferation in vitro and in vivo. by Maruno K, Absood A, Said SI.; 1998 Nov 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24380
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with lung cancer, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “lung cancer” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for lung cancer (hyperlinks lead to article summaries): ·
A 63-year-old man with suspected lung cancer and acute renal failure. Author(s): Papagiannis A, Xafenias A, Kourtoglou G, Zarogoulidis K. Source: Chest. 2003 June; 123(6): 2140-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796200&dopt=Abstract
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A case-case study comparing the usefulness of serum trace elements (Cu, Zn and Se) and tumor markers (CEA, SCC and SLX) in non-small cell lung cancer patients. Author(s): Oyama T, Kawamoto T, Matsuno K, Osaki T, Matsumoto A, Isse T, Nakata S, Ozaki S, Sugaya M, Yasuda M, Yamashita T, Takenoyama M, Sugio K, Yasumoto K. Source: Anticancer Res. 2003 January-February; 23(1B): 605-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680155&dopt=Abstract
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A meta-analysis of asthma and risk of lung cancer (United States). Author(s): Santillan AA, Camargo CA Jr, Colditz GA. Source: Cancer Causes & Control : Ccc. 2003 May; 14(4): 327-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846363&dopt=Abstract
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PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A new irradiation system for lung cancer combining linear accelerator, computed tomography, patient self-breath-holding, and patient-directed beam-control without respiratory monitoring devices. Author(s): Onishi H, Kuriyama K, Komiyama T, Tanaka S, Sano N, Aikawa Y, Tateda Y, Araki T, Ikenaga S, Uematsu M. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 May 1; 56(1): 14-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694819&dopt=Abstract
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A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice. Author(s): Zhang H, Yano S, Miki T, Goto H, Kanematsu T, Muguruma H, Uehara H, Sone S. Source: Clinical & Experimental Metastasis. 2003; 20(2): 153-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705636&dopt=Abstract
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A novel method for sentinel lymph node mapping using magnetite in patients with non-small cell lung cancer. Author(s): Nakagawa T, Minamiya Y, Katayose Y, Saito H, Taguchi K, Imano H, Watanabe H, Enomoto K, Sageshima M, Ueda T, Ogawa J. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 August; 126(2): 563-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928659&dopt=Abstract
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A phase II single-institution study of neoadjuvant stage IIIA/B chemotherapy and radiochemotherapy in non-small cell lung cancer. Author(s): Granetzny A, Striehn E, Bosse U, Wagner W, Koch O, Vogt U, Froeschle P, Klinke F. Source: The Annals of Thoracic Surgery. 2003 April; 75(4): 1107-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683546&dopt=Abstract
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A population-based study of glutathione S-transferase M1, T1 and P1 genotypes and risk for lung cancer. Author(s): Nazar-Stewart V, Vaughan TL, Stapleton P, Van Loo J, Nicol-Blades B, Eaton DL. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 247-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781423&dopt=Abstract
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A prospective study of indications for mediastinoscopy in lung cancer with CT findings, tumor size, and tumor markers. Author(s): Kimura H, Iwai N, Ando S, Kakizawa K, Yamamoto N, Hoshino H, Anayama T. Source: The Annals of Thoracic Surgery. 2003 June; 75(6): 1734-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822608&dopt=Abstract
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A prospective study of infections in lung cancer patients admitted to the hospital. Author(s): Berghmans T, Sculier JP, Klastersky J. Source: Chest. 2003 July; 124(1): 114-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853512&dopt=Abstract
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A prospective study of the impact of weight loss and the systemic inflammatory response on quality of life in patients with inoperable non-small cell lung cancer. Author(s): Scott HR, McMillan DC, Brown DJ, Forrest LM, McArdle CS, Milroy R. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 295-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781428&dopt=Abstract
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A randomized trial of postoperative UFT therapy in p stage I, II non-small cell lung cancer: North-east Japan Study Group for Lung Cancer Surgery. Author(s): Endo C, Saito Y, Iwanami H, Tsushima T, Imai T, Kawamura M, Kondo T, Koike K, Handa M, Kanno R, Fujimura S; North-east Japan Study Group for Lung Cancer Surgery. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 181-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711119&dopt=Abstract
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Aberrant methylation of TMS1 in small cell, non small cell lung cancer and breast cancer. Author(s): Virmani A, Rathi A, Sugio K, Sathyanarayana UG, Toyooka S, Kischel FC, Tonk V, Padar A, Takahashi T, Roth JA, Euhus DM, Minna JD, Gazdar AF. Source: International Journal of Cancer. Journal International Du Cancer. 2003 August 20; 106(2): 198-204. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800194&dopt=Abstract
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Acetone extract of Bupleurum scorzonerifolium inhibits proliferation of A549 human lung cancer cells via inducing apoptosis and suppressing telomerase activity. Author(s): Cheng YL, Chang WL, Lee SC, Liu YG, Lin HC, Chen CJ, Yen CY, Yu DS, Lin SZ, Harn HJ. Source: Life Sciences. 2003 September 19; 73(18): 2383-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941440&dopt=Abstract
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Adenoviral melanoma differentiation-associated gene 7 induces apoptosis in lung cancer cells through mitochondrial permeability transition-independent cytochrome c release. Author(s): Pataer A, Chada S, Hunt KK, Roth JA, Swisher SG. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 June; 125(6): 1328-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830052&dopt=Abstract
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Adjuvant chemotherapy for non-small-cell lung cancer: the end of the beginning. Author(s): Johnson BE. Source: Journal of the National Cancer Institute. 2003 October 1; 95(19): 1422-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519741&dopt=Abstract
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Adjuvant therapy in completely resected non-small-cell lung cancer. Author(s): Scagliotti GV, Novello S. Source: Current Oncology Reports. 2003 July; 5(4): 318-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781075&dopt=Abstract
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Adoptive cellular immunotherapy for non-small cell lung cancer: a pilot study. Author(s): Chan B, Lee W, Hu CX, Ng P, Li KW, Lo G, Ho G, Yeung DW, Woo D. Source: Cytotherapy. 2003; 5(1): 46-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745587&dopt=Abstract
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Aggressive treatment for the fit elderly with non-small-cell lung cancer? Yes! Author(s): Sequist LV, Lynch TJ. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 1; 21(17): 3186-8. Epub 2003 July 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874267&dopt=Abstract
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Allelic loss of DNA locus of the RET proto-oncogene in small cell lung cancer. Author(s): Futami H, Egawa S, Takasaki K, Tsukada T, Shiraishi M, Yamaguchi K. Source: Cancer Letters. 2003 May 30; 195(1): 59-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767512&dopt=Abstract
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Allelic loss on chromosome 3p21.3 and promoter hypermethylation of semaphorin 3B in non-small cell lung cancer. Author(s): Kuroki T, Trapasso F, Yendamuri S, Matsuyama A, Alder H, Williams NN, Kaiser LR, Croce CM. Source: Cancer Research. 2003 June 15; 63(12): 3352-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810670&dopt=Abstract
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Alu profiling of primary and metastatic nonsmall cell lung cancer. Author(s): Furmaga WB, Ryan JL, Coleman WB, Cole SR, Tsongalis GJ. Source: Experimental and Molecular Pathology. 2003 June; 74(3): 224-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782008&dopt=Abstract
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An overview of lung cancer. Author(s): Sachs S, Fiore JJ. Source: Respir Care Clin N Am. 2003 March; 9(1): 1-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820710&dopt=Abstract
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Analysis of NQO1, GSTP1, and MnSOD genetic polymorphisms on lung cancer risk in Taiwan. Author(s): Lin P, Hsueh YM, Ko JL, Liang YF, Tsai KJ, Chen CY. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 123-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711112&dopt=Abstract
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Angiogenesis in the progression of lung cancer. Author(s): Yano S, Goto H, Yamamoto A, Kanematsu T, Sone S. Source: Intern Med. 2003 March; 42(3): 305-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705807&dopt=Abstract
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Appraising the economic efficiency of cancer treatment: an exploratory analysis of lung cancer. Author(s): Chirikos TN. Source: Health Care Management Science. 2003 May; 6(2): 87-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733612&dopt=Abstract
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Assessment of whether in-hospital mortality for lobectomy is a useful standard for the quality of lung cancer surgery: retrospective study. Author(s): Treasure T, Utley M, Bailey A. Source: Bmj (Clinical Research Ed.). 2003 July 12; 327(7406): 73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855523&dopt=Abstract
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Association between glutathione S-transferase p1 polymorphisms and lung cancer risk in Caucasians: a case-control study. Author(s): Wang Y, Spitz MR, Schabath MB, Ali-Osman F, Mata H, Wu X. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 25-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660004&dopt=Abstract
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Association between self-reported environmental tobacco smoke exposure and lung cancer: modification by GSTP1 polymorphism. Author(s): Miller DP, De Vivo I, Neuberg D, Wain JC, Lynch TJ, Su L, Christiani DC. Source: International Journal of Cancer. Journal International Du Cancer. 2003 May 10; 104(6): 758-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640684&dopt=Abstract
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Association of microsomal epoxide hydrolase polymorphisms and lung cancer risk. Author(s): Gsur A, Zidek T, Schnattinger K, Feik E, Haidinger G, Hollaus P, MohnStaudner A, Armbruster C, Madersbacher S, Schatzl G, Trieb K, Vutuc C, Micksche M. Source: British Journal of Cancer. 2003 August 18; 89(4): 702-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915882&dopt=Abstract
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Autocrine motility factor-receptor gene expression in lung cancer. Author(s): Takanami I, Takeuchi K. Source: Jpn J Thorac Cardiovasc Surg. 2003 August; 51(8): 368-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962414&dopt=Abstract
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Balance between cell division and cell death as predictor of survival in patients with non-small-cell lung cancer. Author(s): Puglisi F, Minisini AM, Aprile G, Barbone F, Cataldi P, Artico D, Damante G, Beltrami CA, Di Loreto C. Source: Oncology. 2002; 63(1): 76-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187075&dopt=Abstract
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Bcl-2 determines susceptibility to induction of lung cancer by oncogenic CRaf. Author(s): Fedorov LM, Tyrsin OY, Papadopoulos T, Camarero G, Gotz R, Rapp UR. Source: Cancer Research. 2002 November 1; 62(21): 6297-303. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414660&dopt=Abstract
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Bee venom induces apoptosis and inhibits expression of cyclooxygenase-2 mRNA in human lung cancer cell line NCI-H1299. Author(s): Jang MH, Shin MC, Lim S, Han SM, Park HJ, Shin I, Lee JS, Kim KA, Kim EH, Kim CJ. Source: Journal of Pharmacological Sciences. 2003 February; 91(2): 95-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686753&dopt=Abstract
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Benefits of chemotherapy for quality of life in patients with advanced nonsmall-cell lung cancer. Author(s): Paesmans M. Source: Current Opinion in Oncology. 2002 July; 14(4): 389-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12130921&dopt=Abstract
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Beryllium and lung cancer: a reanalysis of a niosh cohort mortality study. Author(s): Levy PS, Roth HD, Hwang PM, Powers TE. Source: Inhalation Toxicology. 2002 October; 14(10): 1003-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12396408&dopt=Abstract
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Best supportive care versus palliative chemotherapy in nonsmall-cell lung cancer. Author(s): Medley L, Cullen M. Source: Current Opinion in Oncology. 2002 July; 14(4): 384-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12130920&dopt=Abstract
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Biological markers in non-small cell lung cancer. Retrospective study of 10 year follow-up after surgery. Author(s): Carbognani P, Tincani G, Crafa P, Sansebastiano G, Pazzini L, Zoni R, Bobbio A, Rusca M. Source: The Journal of Cardiovascular Surgery. 2002 August; 43(4): 545-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12124571&dopt=Abstract
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Biology of lung cancer with implications for new therapies. Author(s): Aberle MF, McLeskey SW. Source: Oncology Nursing Forum. 2003 March-April; 30(2): 273-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692661&dopt=Abstract
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Bleomycin-induced chromosome breaks as a risk marker for lung cancer: a casecontrol study with population and hospital controls. Author(s): Zheng YL, Loffredo CA, Yu Z, Jones RT, Krasna MJ, Alberg AJ, Yung R, Perlmutter D, Enewold L, Harris CC, Shields PG. Source: Carcinogenesis. 2003 February; 24(2): 269-74. Erratum In: Carcinogenesis. 2003 August; 24(8): 1425. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584177&dopt=Abstract
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Blood glutathione as a surrogate marker of cancer tissue glutathione S-transferase activity in non-small cell lung cancer and squamous cell carcinoma of the head and neck. Author(s): Ferruzzi E, Franceschini R, Cazzolato G, Geroni C, Fowst C, Pastorino U, Tradati N, Tursi J, Dittadi R, Gion M. Source: European Journal of Cancer (Oxford, England : 1990). 2003 May; 39(7): 1019-29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706373&dopt=Abstract
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Blood hemoglobin as an independent prognostic factor in surgically resected stages I and II non-small cell lung cancer patients. Author(s): Watine J. Source: The Annals of Thoracic Surgery. 2002 June; 73(6): 2034-5; Author Reply 2035. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12078827&dopt=Abstract
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Blood pressure, smoking, and the incidence of lung cancer in hypertensive men in North Karelia, Finland. Author(s): Lindgren A, Pukkala E, Nissinen A, Tuomilehto J. Source: American Journal of Epidemiology. 2003 September 1; 158(5): 442-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12936899&dopt=Abstract
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Bone metastasis as the first manifestation of lung cancer. Author(s): Kagohashi K, Satoh H, Ishikawa H, Ohtsuka M, Sekizawa K. Source: Int J Clin Pract. 2003 April; 57(3): 184-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723721&dopt=Abstract
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BRAF and RAS mutations in human lung cancer and melanoma. Author(s): Brose MS, Volpe P, Feldman M, Kumar M, Rishi I, Gerrero R, Einhorn E, Herlyn M, Minna J, Nicholson A, Roth JA, Albelda SM, Davies H, Cox C, Brignell G, Stephens P, Futreal PA, Wooster R, Stratton MR, Weber BL. Source: Cancer Research. 2002 December 1; 62(23): 6997-7000. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460918&dopt=Abstract
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Brain metastasis as the first manifestation of lung cancer. Author(s): Kagohashi K, Satoh H, Yamashita YT, Sekizawa K. Source: The American Journal of Medicine. 2003 April 1; 114(5): 420. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714137&dopt=Abstract
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Breast and lung cancer are associated with a decrease in blood cell amino acid content. Author(s): Proenza AM, Oliver J, Palou A, Roca P. Source: The Journal of Nutritional Biochemistry. 2003 March; 14(3): 133-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742540&dopt=Abstract
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Bronchial hyperresponsiveness in patients with squamous cell lung cancer. Author(s): Inoue R, Nishimura Y, Kado T, Yokoyama M. Source: Respirology (Carlton, Vic.). 2002 December; 7(4): 339-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12421242&dopt=Abstract
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Bronchioloalveolar lung cancer: occurrence, surgical treatment and survival. Author(s): Furak J, Trojan I, Szoke T, Tiszlavicz L, Morvay Z, Eller J, Balogh A. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 May; 23(5): 818-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754039&dopt=Abstract
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Bronchopleural fistula prevention after major pulmonary resection for primary lung cancer. Author(s): Bazzocchi R, Bini A, Grazia M, Petrella F. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2002 July; 22(1): 160. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12103397&dopt=Abstract
78 Lung Cancer
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Bronchoscopic radioisotope injection for sentinel lymph-node mapping in potentially resectable non-small-cell lung cancer. Author(s): Lardinois D, Brack T, Gaspert A, Spahr T, Schneiter D, Steinert HC, Weder W. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 May; 23(5): 824-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754040&dopt=Abstract
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Bronchoscopic treatment of patients with intraluminal microinvasive radiographically occult lung cancer not eligible for surgical resection: a follow-up study. Author(s): Vonk-Noordegraaf A, Postmus PE, Sutedja TG. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 49-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499094&dopt=Abstract
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Case-control study of lung cancer during 1994-1997 in the birth cohort in Tasmania, Australia, with an excess of female cases during 1983-1992. Author(s): Blizzard L, Dwyer T. Source: Cancer Causes & Control : Ccc. 2003 March; 14(2): 123-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749717&dopt=Abstract
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Changes in hemodynamics in patients who underwent extended mediastinal lymphadenectomy through median sternotomy for primary lung cancer. Author(s): Hirata T, Koizumi K, Tanaka S. Source: Jpn J Thorac Cardiovasc Surg. 2003 May; 51(5): 178-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776948&dopt=Abstract
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Chemoprevention in lung cancer. Author(s): Reddy SC, Khuri FR. Source: J Med Assoc Ga. 2003 Winter-Spring; 92(1): 27-33. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743903&dopt=Abstract
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Chemotherapy options for the elderly patient with advanced non-small cell lung cancer. Author(s): Hennessy BT, Hanrahan EO, Breathnach OS. Source: The Oncologist. 2003; 8(3): 270-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12773749&dopt=Abstract
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Chemotherapy versus best supportive care in the management of lung cancer. Author(s): Shajeem O, Behera D, Aggarwal AN. Source: J Assoc Physicians India. 2003 March; 51: 261-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839347&dopt=Abstract
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Chilean pilot study on the risk of lung cancer associated with codon 72 polymorphism in the gene of protein p53. Author(s): Irarrazabal CE, Rojas C, Aracena R, Marquez C, Gil L. Source: Toxicology Letters. 2003 September 15; 144(1): 69-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12919725&dopt=Abstract
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Chronic Chlamydophila pneumoniae infection in lung cancer, a risk factor: a casecontrol study. Author(s): Kocazeybek B. Source: Journal of Medical Microbiology. 2003 August; 52(Pt 8): 721-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867569&dopt=Abstract
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Clinical efficacy and toxicity of gefitinib in patients with lung cancer. Author(s): Teramoto S, Yamamoto H, Ouchi Y. Source: Lancet. 2003 June 7; 361(9373): 1992-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801775&dopt=Abstract
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Clinical efficacy and toxiciy of gefitinib in patients with lung cancer. Author(s): Mitsui H, Nakajima J, Maruyama T, Hanajiri K, Omata M. Source: Lancet. 2003 June 7; 361(9373): 1993. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801776&dopt=Abstract
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Clinical equivalence of two cytokeratin markers in mon-small cell lung cancer: a study of tissue polypeptide antigen and cytokeratin 19 fragments. Author(s): Buccheri G, Torchio P, Ferrigno D. Source: Chest. 2003 August; 124(2): 622-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907552&dopt=Abstract
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Clinical significance of co-expression of VEGF-C and VEGFR-3 in non-small cell lung cancer. Author(s): Li Q, Dong X, Gu W, Qiu X, Wang E. Source: Chin Med J (Engl). 2003 May; 116(5): 727-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875690&dopt=Abstract
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Clinical value of CEA and CA125 regarding relapse and metastasis in resectable nonsmall cell lung cancer. Author(s): Gaspar MJ, Diez M, Rodriguez A, Ratia T, Martin Duce A, Galvan M, Granell J, Coca C. Source: Anticancer Res. 2003 July-August; 23(4): 3427-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926084&dopt=Abstract
80 Lung Cancer
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Combination of low-dose cisplatin and gemcitabine for treatment of elderly patients with advanced non-small-cell lung cancer. Author(s): Feliu J, Martin G, Madronal C, Rodriguez-Jaraiz A, Castro J, Rodriguez A, Checa T, Bolano M, Casado E, Gonzalez-Baron M. Source: Cancer Chemotherapy and Pharmacology. 2003 September; 52(3): 247-52. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783203&dopt=Abstract
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Combined modality therapy of early stage nonsmall cell lung cancer. Author(s): Pisters KM. Source: Respir Care Clin N Am. 2003 June; 9(2): 191-205. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911289&dopt=Abstract
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Combined therapy with topotecan and gemcitabine in patients with inoperable or metastatic non-small cell lung cancer. Author(s): Dabrow MB, Francesco MR, Gilman PB, Cantor R, Rose L, Meyer TJ. Source: Cancer Investigation. 2003; 21(4): 517-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14533441&dopt=Abstract
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Combined treatment for limited small cell lung cancer. Author(s): Komaki R. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 9): 56-70. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908137&dopt=Abstract
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Computed tomographic screening for lung cancer: home run or foul ball? Author(s): Swensen SJ, Jett JR, Midthun DE, Hartman TE. Source: Mayo Clinic Proceedings. 2003 September; 78(9): 1187-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962174&dopt=Abstract
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Concordant expression of the telomerase-associated genes in non-small cell lung cancer. Author(s): Hsu CP, Miaw J, Hsia JY, Shai SE, Chen CY. Source: European Journal of Surgical Oncology : the Journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology. 2003 September; 29(7): 594-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943625&dopt=Abstract
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Concurrent chemoradiotherapy for inoperable stage III non-small-cell lung cancer. Author(s): MacRae R, Choy H. Source: Current Oncology Reports. 2003 July; 5(4): 313-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781074&dopt=Abstract
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Conditional survival of patients with the four major histologic subgroups of lung cancer in Denmark. Author(s): Skuladottir H, Olsen JH. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3035-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915592&dopt=Abstract
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Coriolus versicolor polysaccharide peptide slows progression of advanced non-small cell lung cancer. Author(s): Tsang KW, Lam CL, Yan C, Mak JC, Ooi GC, Ho JC, Lam B, Man R, Sham JS, Lam WK. Source: Respiratory Medicine. 2003 June; 97(6): 618-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814145&dopt=Abstract
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Correlation between perioperative blood transfusion and prognosis of patients subjected to surgery for stage I lung cancer. Author(s): Nosotti M, Rebulla P, Riccardi D, Baisi A, Bellaviti N, Rosso L, Santambrogio L. Source: Chest. 2003 July; 124(1): 102-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853510&dopt=Abstract
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Cost-effectiveness and lung cancer clinical trials. Author(s): Du W, Reeves JH, Gadgeel S, Abrams J, Peters WP. Source: Cancer. 2003 October 1; 98(7): 1491-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508837&dopt=Abstract
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Cost-effectiveness of screening for lung cancer. Author(s): Chirikos TN, Hazelton T, Tockman M, Clark R. Source: Jama : the Journal of the American Medical Association. 2003 May 14; 289(18): 2358; Author Reply 2358-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746351&dopt=Abstract
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Cost-effectiveness of screening for lung cancer. Author(s): Petty TL. Source: Jama : the Journal of the American Medical Association. 2003 May 14; 289(18): 2357; Author Reply 2358-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746350&dopt=Abstract
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Cost-effectiveness of screening for lung cancer. Author(s): Reich J. Source: Jama : the Journal of the American Medical Association. 2003 May 14; 289(18): 2357; Author Reply 2358-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746349&dopt=Abstract
82 Lung Cancer
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CT screening for lung cancer. Author(s): Yankelevitz D. Source: Ajr. American Journal of Roentgenology. 2003 June; 180(6): 1736-7; Author Reply 1737. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760953&dopt=Abstract
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Current concepts in the mediastinal lymph node staging of nonsmall cell lung cancer. Author(s): Kramer H, Groen HJ. Source: Annals of Surgery. 2003 August; 238(2): 180-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894010&dopt=Abstract
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Cyclin D1 gene polymorphism and susceptibility to lung cancer in a Chinese population. Author(s): Qiuling S, Yuxin Z, Suhua Z, Cheng X, Shuguang L, Fengsheng H. Source: Carcinogenesis. 2003 September; 24(9): 1499-503. Epub 2003 March 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807740&dopt=Abstract
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Cyclin D1 overexpression in bronchial epithelia of patients with lung cancer is associated with smoking and predicts survival. Author(s): Ratschiller D, Heighway J, Gugger M, Kappeler A, Pirnia F, Schmid RA, Borner MM, Betticher DC. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2085-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775733&dopt=Abstract
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Cyclooxygenase-2 in lung cancer. Author(s): Dubinett SM, Sharma S, Huang M, Dohadwala M, Pold M, Mao JT. Source: Prog Exp Tumor Res. 2003; 37: 138-62. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12795053&dopt=Abstract
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CYP1A1 and GSTM1 genetic polymorphisms and lung cancer risk in Caucasian nonsmokers: a pooled analysis. Author(s): Hung RJ, Boffetta P, Brockmoller J, Butkiewicz D, Cascorbi I, Clapper ML, Garte S, Haugen A, Hirvonen A, Anttila S, Kalina I, Le Marchand L, London SJ, Rannug A, Romkes M, Salagovic J, Schoket B, Gaspari L, Taioli E. Source: Carcinogenesis. 2003 May; 24(5): 875-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771031&dopt=Abstract
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CYP3A5*1 is an inhibitory factor for lung cancer in Taiwanese. Author(s): Yeh KT, Chen JC, Chen CM, Wang YF, Lee TP, Chang JG. Source: Kaohsiung J Med Sci. 2003 May; 19(5): 201-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822676&dopt=Abstract
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Daily activities: exploring their spectrum and prognostic impact in older, chemotherapy-treated lung cancer patients. Author(s): Jatoi A, Hillman S, Stella PJ, Mailliard JA, Sloan J, Vanone S, Cannon MW, Kutteh L, Kanard A, Jett JR. Source: Supportive Care in Cancer : Official Journal of the Multinational Association of Supportive Care in Cancer. 2003 July; 11(7): 460-4. Epub 2003 March 12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14505160&dopt=Abstract
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Daily low-dose cisplatin and concurrent thoracic irradiation for poor-risk patients with unresectable non-small-cell lung cancer. Author(s): Takata I, Ueoka H, Kiura K, Tabata M, Takigawa N, Katayama H, Takemoto M, Hiraki Y, Harada M, Tanimoto M. Source: Acta Medica Okayama. 2002 October; 56(5): 261-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530510&dopt=Abstract
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DEC1 (STRA13) protein expression relates to hypoxia- inducible factor 1-alpha and carbonic anhydrase-9 overexpression in non-small cell lung cancer. Author(s): Giatromanolaki A, Koukourakis MI, Sivridis E, Turley H, Wykoff CC, Gatter KC, Harris AL. Source: The Journal of Pathology. 2003 June; 200(2): 222-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754744&dopt=Abstract
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Declining sex differences in mortality from lung cancer in high-income nations. Author(s): Pampel FC. Source: Demography. 2003 February; 40(1): 45-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12647513&dopt=Abstract
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Defining the need for radiotherapy for lung cancer in the general population: a criterion-based, benchmarking approach. Author(s): Barbera L, Zhang-Salomons J, Huang J, Tyldesley S, Mackillop W. Source: Medical Care. 2003 September; 41(9): 1074-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972847&dopt=Abstract
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Dendritic cells efficiently acquire and present antigen derived from lung cancer cells and induce antigen-specific T-cell responses. Author(s): Zhou Y, McEarchern JA, Howard E, Pestano G, Salgaller ML, Bosch ML. Source: Cancer Immunology, Immunotherapy : Cii. 2003 July; 52(7): 413-22. Epub 2003 February 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835918&dopt=Abstract
84 Lung Cancer
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Depression and psychological distress in patients during the year after curative resection of non-small-cell lung cancer. Author(s): Uchitomi Y, Mikami I, Nagai K, Nishiwaki Y, Akechi T, Okamura H. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 January 1; 21(1): 69-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506173&dopt=Abstract
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Detailed characterization of a homozygously deleted region corresponding to a candidate tumor suppressor locus at distal 17p13.3 in human lung cancer. Author(s): Konishi H, Sugiyama M, Mizuno K, Saito H, Yatabe Y, Takahashi T, Osada H, Takahashi T. Source: Oncogene. 2003 March 27; 22(12): 1892-905. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660825&dopt=Abstract
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Detection of loss of heterozygosity by high-resolution fluorescent system in nonsmall cell lung cancer: association of loss of heterozygosity with smoking and tumor progression. Author(s): Yoshino I, Fukuyama S, Kameyama T, Shikada Y, Oda S, Maehara Y, Sugimachi K. Source: Chest. 2003 February; 123(2): 545-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576379&dopt=Abstract
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Detection of lung cancer with volatile markers in the breath. Author(s): Phillips M, Cataneo RN, Cummin AR, Gagliardi AJ, Gleeson K, Greenberg J, Maxfield RA, Rom WN. Source: Chest. 2003 June; 123(6): 2115-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796197&dopt=Abstract
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Detection of telomerase activity in bronchial lavage as an adjunct to cytological diagnosis in lung cancer. Author(s): Dikmen E, Kara M, Dikmen G, Cakmak H, Dogan P. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 February; 23(2): 194-9; Discussion 199-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559342&dopt=Abstract
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Detection of telomerase expression in mediastinal lymph nodes of patients with lung cancer. Author(s): Wallace MB, Block M, Hoffman BJ, Hawes RH, Silvestri G, Reed CE, Mitas M, Ravenel J, Fraig M, Miller S, Jones ET, Boylan A. Source: American Journal of Respiratory and Critical Care Medicine. 2003 June 15; 167(12): 1670-5. Epub 2003 February 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615614&dopt=Abstract
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Development of brain metastasis 5 years before the appearance of the primary lung cancer: “messenger metachronous metastasis”. Author(s): Furak J, Trojan I, Tiszlavicz L, Micsik T, Puskas LG. Source: The Annals of Thoracic Surgery. 2003 March; 75(3): 1016-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645740&dopt=Abstract
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Diagnosis and management of lung cancer: ACCP evidence-based guidelines. American College of Chest Physicians. Author(s): American College of Chest Physicians; Health and Science Policy Committee. Source: Chest. 2003 January; 123(1 Suppl): D-G, 1S-337S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527560&dopt=Abstract
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Diagnosis of lung cancer: the guidelines. Author(s): Rivera MP, Detterbeck F, Mehta AC; American College of Chest Physicians. Source: Chest. 2003 January; 123(1 Suppl): 129S-136S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527572&dopt=Abstract
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Diagnostic challenges in patients with tumors: case 2. Staphylococcal scalded-skin syndrome in a patient with extended small-cell lung cancer. Author(s): Longo R, Amici S, Carillio G, Gasparini G. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3702-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512404&dopt=Abstract
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Diagnostic value of plasma vascular endothelial growth factor as a tumor marker in patients with non-small cell lung cancer. Author(s): Tamura M, Ohta Y, Nakamura H, Oda M, Watanabe G. Source: Int J Biol Markers. 2002 October-December; 17(4): 275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521132&dopt=Abstract
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Dietary carotenoids, vegetables, and lung cancer risk in women: the Missouri women's health study (United States). Author(s): Wright ME, Mayne ST, Swanson CA, Sinha R, Alavanja MC. Source: Cancer Causes & Control : Ccc. 2003 February; 14(1): 85-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708729&dopt=Abstract
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Different measures of asbestos exposure in estimating risk of lung cancer and mesothelioma among construction workers. Author(s): Koskinen K, Pukkala E, Martikainen R, Reijula K, Karjalainen A. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2002 December; 44(12): 1190-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12500463&dopt=Abstract
86 Lung Cancer
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Different risk relations with smoking for non-small-cell lung cancer: comparison of TP53 and TP73 genotypes. Author(s): Hiraki A, Matsuo K, Hamajima N, Ito H, Hatooka S, Suyama M, Mitsudomi T, Tajima K. Source: Asian Pac J Cancer Prev. 2003 April-June; 4(2): 107-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875622&dopt=Abstract
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Diffuse alveolar damage after ZD1839 therapy in a patient with non-small cell lung cancer. Author(s): Okamoto I, Fujii K, Matsumoto M, Terasaki Y, Kihara N, Kohrogi H, Suga M. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 339-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781434&dopt=Abstract
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Diffusely increased uptake by thoracic vertebrae on bone scintigraphy in midcourse of lung cancer irradiation: a case report. Author(s): Shih WJ, Gross K. Source: Journal of Nuclear Medicine Technology. 2003 June; 31(2): 79-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12777458&dopt=Abstract
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Dihydropyrimidine dehydrogenase levels in nonsmall-cell lung cancer tissues. Author(s): Yano T, Koga T, Ninomiya S, Takeo S. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2002 December; 7(6): 361-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12494252&dopt=Abstract
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Direct treatment costs for patients with lung cancer from first recurrence to death in france. Author(s): Braud AC, Levy-Piedbois C, Piedbois P, Piedbois Y, Livartovski A, Le Vu B, Tredaniel J, Reboul F, Brewer Y, Talbi S, Blanchon F, Paschen B, Durand-Zaleski I. Source: Pharmacoeconomics. 2003; 21(9): 671-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807368&dopt=Abstract
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Discrepancy between Tc-99m HMDP bone scan and F-18 FDG positron emission tomographic images in a patient with small cell lung cancer. Author(s): Fukuchi K, Yamaguchi M, Hayashida K, Ishida Y. Source: Clinical Nuclear Medicine. 2003 March; 28(3): 232-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592136&dopt=Abstract
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Disseminated Actinomyces meyeri infection resembling lung cancer with brain metastases. Author(s): Colmegna I, Rodriguez-Barradas M, Rauch R, Clarridge J, Young EJ. Source: The American Journal of the Medical Sciences. 2003 September; 326(3): 152-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501233&dopt=Abstract
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DNA repair activity for oxidative damage and risk of lung cancer. Author(s): Paz-Elizur T, Krupsky M, Blumenstein S, Elinger D, Schechtman E, Livneh Z. Source: Journal of the National Cancer Institute. 2003 September 3; 95(17): 1312-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953085&dopt=Abstract
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Do newly diagnosed lung cancer patients feel their concerns are being met? Author(s): Hill KM, Amir Z, Muers MF, Connolly CK, Round CE. Source: European Journal of Cancer Care. 2003 March; 12(1): 35-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12641555&dopt=Abstract
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Does HIV adversely influence the outcome in advanced non-small-cell lung cancer in the era of HAART? Author(s): Powles T, Thirwell C, Newsom-Davis T, Nelson M, Shah P, Cox S, Gazzard B, Bower M. Source: British Journal of Cancer. 2003 August 4; 89(3): 457-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888811&dopt=Abstract
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Dose-comparative monotherapy trials of ZD1839 in previously treated non-small cell lung cancer patients. Author(s): Herbst RS. Source: Seminars in Oncology. 2003 February; 30(1 Suppl 1): 30-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644982&dopt=Abstract
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Dose-escalation with CHARTWEL (continuous hyperfractionated accelerated radiotherapy week-end less) combined with neo-adjuvant chemotherapy in the treatment of locally advanced non-small cell lung cancer. Author(s): Saunders MI, Rojas A, Lyn BE, Wilson E, Phillips H. Source: Clin Oncol (R Coll Radiol). 2002 October; 14(5): 352-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555873&dopt=Abstract
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Downregulation of plasma membrane expression/cytoplasmic accumulation of betacatenin predicts shortened survival in non-small cell lung cancer. A clinicopathologic study of 100 cases. Author(s): Kren L, Hermanova M, Goncharuk VN, Kaur P, Ross JS, Pavlovsky Z, Dvorak K. Source: Cesk Patol. 2003 January; 39(1): 17-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673938&dopt=Abstract
88 Lung Cancer
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Early detection of lung cancer: role of biomarkers. Author(s): Brambilla C, Fievet F, Jeanmart M, de Fraipont F, Lantuejoul S, Frappat V, Ferretti G, Brichon PY, Moro-Sibilot D. Source: Eur Respir J Suppl. 2003 January; 39: 36S-44S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572700&dopt=Abstract
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Early lung cancer action project pathology protocol. Author(s): Vazquez M, Flieder D, Travis W, Carter D, Yankelevitz DF, Miettinen OS, Henschke CI. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 231-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581579&dopt=Abstract
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Economic status, smoking, occupational exposure to rubber, and lung cancer: a casecohort study. Author(s): Li K, Yu S. Source: Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews. 2002 May; 20(1): 21-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734051&dopt=Abstract
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Economic, legal, and ethical rationales for the ACRIN national lung screening trial of CT screening for lung cancer. Author(s): Hillman BJ; ACRIN. Source: Academic Radiology. 2003 March; 10(3): 349-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643562&dopt=Abstract
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Effect of epoxide hydrolase polymorphisms on chromosome aberrations and risk for lung cancer. Author(s): Cajas-Salazar N, Au WW, Zwischenberger JB, Sierra-Torres CH, Salama SA, Alpard SK, Tyring SK. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 97-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935919&dopt=Abstract
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Effect of number of lymph nodes sampled on outcome in patients with stage I nonsmall-cell lung cancer. Author(s): Gajra A, Newman N, Gamble GP, Kohman LJ, Graziano SL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 March 15; 21(6): 1029-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637467&dopt=Abstract
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Effect of radioisotope sentinel node mapping in patients with cT1 N0 M0 lung cancer. Author(s): Sugi K, Kaneda Y, Sudoh M, Sakano H, Hamano K. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 August; 126(2): 56873. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928660&dopt=Abstract
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Effect of temporal subtraction technique on the diagnosis of primary lung cancer with chest radiography. Author(s): Matsuda T, Yasuhara Y, Kano A, Mochizuki T, Ikezoe J. Source: Radiat Med. 2003 May-June; 21(3): 112-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12868859&dopt=Abstract
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Efficacy and safety of zoledronic acid in the treatment of bone metastases associated with lung cancer and other solid tumors. Author(s): Rosen LS. Source: Seminars in Oncology. 2002 December; 29(6 Suppl 21): 28-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584692&dopt=Abstract
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Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. Author(s): Kris MG, Natale RB, Herbst RS, Lynch TJ Jr, Prager D, Belani CP, Schiller JH, Kelly K, Spiridonidis H, Sandler A, Albain KS, Cella D, Wolf MK, Averbuch SD, Ochs JJ, Kay AC. Source: Jama : the Journal of the American Medical Association. 2003 October 22; 290(16): 2149-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14570950&dopt=Abstract
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Efficacy of neoadjuvant strategies with gemcitabine and other chemotherapy in resectable non-small cell lung cancer: a combined modality approach. Author(s): Scagliotti GV, Novello S. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 10): 13-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917816&dopt=Abstract
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Elevated levels of intracellular Ca2+ and apoptosis in human lung cancer cells given heat-shock. Author(s): Hashimoto T, Shibata MA, Ito Y, Nakao KI, Sasaki S, Otsuki Y. Source: International Journal of Hyperthermia : the Official Journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group. 2003 March-April; 19(2): 178-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623640&dopt=Abstract
90 Lung Cancer
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Elevated serum epidermal growth factor receptor level is correlated with lymph node metastasis in lung cancer. Author(s): Sasaki H, Yukiue H, Mizuno K, Sekimura A, Konishi A, Yano M, Kaji M, Kiriyama M, Fukai I, Yamakawa Y, Fujii Y. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2003 April; 8(2): 79-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12720099&dopt=Abstract
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Elevated serum periostin levels in patients with bone metastases from breast but not lung cancer. Author(s): Sasaki H, Yu CY, Dai M, Tam C, Loda M, Auclair D, Chen LB, Elias A. Source: Breast Cancer Research and Treatment. 2003 February; 77(3): 245-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602924&dopt=Abstract
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En-bloc chest wall and lung resection for non-small cell lung cancer. Predictors of 60day non-cancer related mortality. Author(s): Martin-Ucar AE, Nicum R, Oey I, Edwards JG, Waller DA. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 June; 23(6): 859-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829058&dopt=Abstract
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Environmental exposure and lung cancer among nonsmokers: an example of Taiwanese female lung cancer. Author(s): Wen Cheng Y, Lee H. Source: Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews. 2003 May; 21(1): 1-28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826030&dopt=Abstract
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Epidemiological associations among lung cancer, radon exposure and elevation above sea level--a reassessment of Cohen's county level radon study. Author(s): Van Pelt WR. Source: Health Physics. 2003 October; 85(4): 397-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13678279&dopt=Abstract
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Epidemiology of lung cancer. Author(s): Kollarova H, Janout V, Cizek L. Source: Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2002 December; 146(2): 103-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572908&dopt=Abstract
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Epidermal growth factor receptor, cyclooxygenase-2, and BAX expression in the primary non-small cell lung cancer and brain metastases. Author(s): Milas I, Komaki R, Hachiya T, Bubb RS, Ro JY, Langford L, Sawaya R, Putnam JB, Allen P, Cox JD, McDonnell TJ, Brock W, Hong WK, Roth JA, Milas L. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 March; 9(3): 1070-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631609&dopt=Abstract
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Erlotinib: a new therapeutic approach for non-small cell lung cancer. Author(s): Bonomi P. Source: Expert Opinion on Investigational Drugs. 2003 August; 12(8): 1395-401. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882624&dopt=Abstract
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Evaluation of cumulative prognostic scores based on the systemic inflammatory response in patients with inoperable non-small-cell lung cancer. Author(s): Forrest LM, McMillan DC, McArdle CS, Angerson WJ, Dunlop DJ. Source: British Journal of Cancer. 2003 September 15; 89(6): 1028-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966420&dopt=Abstract
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Evaluation of different markers in non-small cell lung cancer: prognostic value of clinical staging, tumour cell detection and tumour marker analysis for tumour progression and overall survival. Author(s): Kasimir-Bauer S, Schleucher N, Weber R, Neumann R, Seeber S. Source: Oncol Rep. 2003 March-April; 10(2): 475-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579292&dopt=Abstract
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Evidence that phosphatidylinositol 3-kinase- and mitogen-activated protein kinase kinase-4/c-Jun NH2-terminal kinase-dependent Pathways cooperate to maintain lung cancer cell survival. Author(s): Lee HY, Srinivas H, Xia D, Lu Y, Superty R, LaPushin R, Gomez-Manzano C, Gal AM, Walsh GL, Force T, Ueki K, Mills GB, Kurie JM. Source: The Journal of Biological Chemistry. 2003 June 27; 278(26): 23630-8. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714585&dopt=Abstract
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Evidence-based follow-up of lung cancer patients. Author(s): Smith TJ. Source: Seminars in Oncology. 2003 June; 30(3): 361-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870137&dopt=Abstract
92 Lung Cancer
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Evidence-based prevention (EBP): approach to lung cancer prevention based on cytochrome 1A1 and cytochrome 2E1 polymorphism. Author(s): Oyama T, Matsumoto A, Isse T, Kim YD, Ozaki S, Osaki T, Sugio K, Yasumoto K, Kawamoto T. Source: Anticancer Res. 2003 March-April; 23(2C): 1731-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820449&dopt=Abstract
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Examining the effects of false positive lung cancer screening results on subsequent lung cancer screening adherence. Author(s): Ford ME, Havstad SL, Flickinger L, Johnson CC. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2003 January; 12(1): 28-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540500&dopt=Abstract
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Expression of aphidicolin-induced fragile sites and their relationship between genetic susceptibility in breast cancer, ovarian cancer, and non-small-cell lung cancer patients. Author(s): Dhillon VS, Husain SA, Ray GN. Source: Teratogenesis, Carcinogenesis, and Mutagenesis. 2003; Suppl 1: 35-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12616595&dopt=Abstract
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Expression of apoptosis-related proteins and morphological changes in a rat tumor model of human small cell lung cancer prior to and after treatment with radiotherapy, carboplatin, or combined treatment. Author(s): Fokkema E, De Vries EG, Groen HJ, Meijer C, Timens W. Source: Virchows Archiv : an International Journal of Pathology. 2003 April; 442(4): 34955. Epub 2003 February 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715170&dopt=Abstract
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Expression of constitutively activated EGFRvIII in non-small cell lung cancer. Author(s): Okamoto I, Kenyon LC, Emlet DR, Mori T, Sasaki J, Hirosako S, Ichikawa Y, Kishi H, Godwin AK, Yoshioka M, Suga M, Matsumoto M, Wong AJ. Source: Cancer Science. 2003 January; 94(1): 50-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708474&dopt=Abstract
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Expression of endoplasmic reticulum molecular chaperon GRP94 in human lung cancer tissues and its clinical significance. Author(s): Wang Q, An L, Chen Y, Yue S. Source: Chin Med J (Engl). 2002 November; 115(11): 1615-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12609072&dopt=Abstract
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Expression of surface protein receptors in lung cancer. Author(s): Esposito V, Groeger AM, De Luca L, Di Marino M, Santini D, Marchei P, Baldi F, Wolner E, Baldi A. Source: Anticancer Res. 2002 November-December; 22(6C): 4039-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553029&dopt=Abstract
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Expression of tetraspanins in human lung cancer cells: frequent downregulation of CD9 and its contribution to cell motility in small cell lung cancer. Author(s): Funakoshi T, Tachibana I, Hoshida Y, Kimura H, Takeda Y, Kijima T, Nishino K, Goto H, Yoneda T, Kumagai T, Osaki T, Hayashi S, Aozasa K, Kawase I. Source: Oncogene. 2003 February 6; 22(5): 674-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569360&dopt=Abstract
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Expression, proliferation activity and clinical significance of cathepsin B and cathepsin L in operated lung cancer. Author(s): Kayser K, Richter N, Hufnagl P, Kayser G, Kos J, Werle B. Source: Anticancer Res. 2003 May-June; 23(3C): 2767-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926111&dopt=Abstract
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Extension of the “hygiene hypothesis” to the association of occupational endotoxin exposure with lower lung cancer risk. Author(s): Lange JH, Rylander R, Fedeli U, Mastrangelo G. Source: The Journal of Allergy and Clinical Immunology. 2003 July; 112(1): 219-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847509&dopt=Abstract
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Extracts of lung cancer cells reveal antitumour antibodies in sera of patients with lung cancer. Author(s): Bazhin AV, Savchenko MS, Shifrina ON, Chikina SY, Goncharskaia, Jaques G, Chuchalin AG, Philippov PP. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 February; 21(2): 342-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12608451&dopt=Abstract
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Factors influencing the use of thoracic radiotherapy in lung cancer--an analysis of the 1995 Scottish lung cancer audit. Author(s): Erridge SC, Thomson CS, Davidson J, Jones RD, Price A; Scottish Cancer Trials Lung Group and The Scottish Cancer Therapy Network. Source: Clin Oncol (R Coll Radiol). 2002 June; 14(3): 219-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109826&dopt=Abstract
94 Lung Cancer
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Failure of T stage to predict survival in patients with non-small-cell lung cancer treated by radiotherapy with or without concomitant chemotherapy. Author(s): Ball D, Smith J, Wirth A, Mac Manus M. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 November 15; 54(4): 1007-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419426&dopt=Abstract
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Failure to diagnose lung cancer: anatomy of a malpractice trial. Author(s): Berlin L. Source: Ajr. American Journal of Roentgenology. 2003 January; 180(1): 37-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490474&dopt=Abstract
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Farnesol for aerosol inhalation: nebulization and activity against human lung cancer cells. Author(s): Wang Z, Chen HT, Roa W, Finlay W. Source: Journal of Pharmacy & Pharmaceutical Sciences [electronic Resource] : a Publication of the Canadian Society for Pharmaceutical Sciences, Societe Canadienne Des Sciences Pharmaceutiques. 2003 January-April; 6(1): 95-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12753732&dopt=Abstract
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FDA announces fast track approval of new drug for lung cancer. Author(s): Dyer O. Source: Bmj (Clinical Research Ed.). 2003 May 10; 326(7397): 1004. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742913&dopt=Abstract
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FDG-PET imaging in lung cancer: how sensitive is it for bronchioloalveolar carcinoma? Author(s): Yap CS, Schiepers C, Fishbein MC, Phelps ME, Czernin J. Source: European Journal of Nuclear Medicine and Molecular Imaging. 2002 September; 29(9): 1166-73. Epub 2002 June 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12192561&dopt=Abstract
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FDG-PET-detected extracranial metastasis in patients with non-small cell lung cancer undergoing staging for surgery or radical radiotherapy--survival correlates with metastatic disease burden. Author(s): MacManus MR, Hicks R, Fisher R, Rischin D, Michael M, Wirth A, Ball DL. Source: Acta Oncologica (Stockholm, Sweden). 2003; 42(1): 48-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665331&dopt=Abstract
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Feasibility of induction chemotherapy using bronchial arterial infusion for locally advanced non-small cell lung cancer: a pilot study. Author(s): Osaki T, Oyama T, Takenoyama M, Taga S, So T, Yamashita T, Nakata S, Nakanishi R, Yasumoto K. Source: Surgery Today. 2002; 32(9): 772-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12203053&dopt=Abstract
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Fluorescent microsatellite analysis in bronchial lavage as a potential diagnostic tool for lung cancer. Author(s): Field JK, Liloglou T. Source: Methods in Molecular Medicine. 2003; 75: 251-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407745&dopt=Abstract
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Focus on lung cancer. Author(s): Minna JD, Roth JA, Gazdar AF. Source: Cancer Cell. 2002 February; 1(1): 49-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12086887&dopt=Abstract
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Follow-up and surveillance of the lung cancer patient following curative-intent therapy. Author(s): Colice GL, Rubins J, Unger M; American College of Chest Physicians. Source: Chest. 2003 January; 123(1 Suppl): 272S-283S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527585&dopt=Abstract
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Food groups and risk of lung cancer in Uruguay. Author(s): De Stefani E, Brennan P, Ronco A, Fierro L, Correa P, Boffetta P, DeneoPellegrini H, Barrios E. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 1-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367786&dopt=Abstract
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Fractional allele loss is a valuable marker for human lung cancer detection in sputum. Author(s): Arvanitis DA, Papadakis E, Zafiropoulos A, Spandidos DA. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 55-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660007&dopt=Abstract
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Fractionated irradiation of H69 small-cell lung cancer cells causes stable radiation and drug resistance with increased MRP1, MRP2, and topoisomerase IIalpha expression. Author(s): Henness S, Davey MW, Harvie RM, Davey RA. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 November 1; 54(3): 895-902. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377343&dopt=Abstract
96 Lung Cancer
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Fragile histidine triad protein expression in nonsmall cell lung cancer and correlation with Ki-67 and with p53. Author(s): Mascaux C, Martin B, Verdebout JM, Meert AP, Ninane V, Sculier JP. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 May; 21(5): 753-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765416&dopt=Abstract
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Frequent hypermethylation of the 5' CpG island of the mitotic stress checkpoint gene Chfr in colorectal and non-small cell lung cancer. Author(s): Corn PG, Summers MK, Fogt F, Virmani AK, Gazdar AF, Halazonetis TD, ElDeiry WS. Source: Carcinogenesis. 2003 January; 24(1): 47-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538348&dopt=Abstract
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From CHART to CHARTWEL in non-small cell lung cancer: clinical radiobiological modelling of the expected change in outcome. Author(s): Bentzen SM, Saunders MI, Dische S. Source: Clin Oncol (R Coll Radiol). 2002 October; 14(5): 372-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555876&dopt=Abstract
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From clinical and pathologic to molecular staging of lung cancer. Author(s): Massion PP, Carbone DP. Source: American Journal of Respiratory and Critical Care Medicine. 2003 June 15; 167(12): 1587-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796051&dopt=Abstract
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Functional cloning of a tumor suppressor gene, TSLC1, in human non-small cell lung cancer. Author(s): Murakami Y. Source: Oncogene. 2002 October 7; 21(45): 6936-48. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12362275&dopt=Abstract
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Functional genomics in lung cancer and biomarker detection. Author(s): Rom WN, Tchou-Wong KM. Source: American Journal of Respiratory Cell and Molecular Biology. 2003 August; 29(2): 153-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878582&dopt=Abstract
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Fuzzy logic-based tumor marker profiles including a new marker tumor M2-PK improved sensitivity to the detection of progression in lung cancer patients. Author(s): Schneider J, Peltri G, Bitterlich N, Neu K, Velcovsky HG, Morr H, Katz N, Eigenbrodt E. Source: Anticancer Res. 2003 March-April; 23(2A): 899-906. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820320&dopt=Abstract
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Fuzzy logic-based tumor-marker profiles improved sensitivity in the diagnosis of lung cancer. Author(s): Schneider J, Bitterlich N, Velcovsky HG, Morr H, Katz N, Eigenbrodt E. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2002 June; 7(3): 145-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109515&dopt=Abstract
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Gamma knife radiosurgery for metastatic brain tumors from lung cancer: a comparison between small cell and non-small cell carcinoma. Author(s): Serizawa T, Ono J, Iichi T, Matsuda S, Sato M, Odaki M, Hirai S, Osato K, Saeki N, Yamaura A. Source: Journal of Neurosurgery. 2002 December; 97(5 Suppl): 484-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507082&dopt=Abstract
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Gefitinib in pretreated non-small-cell lung cancer (NSCLC): analysis of efficacy and correlation with HER2 and epidermal growth factor receptor expression in locally advanced or metastatic NSCLC. Author(s): Cappuzzo F, Gregorc V, Rossi E, Cancellieri A, Magrini E, Paties CT, Ceresoli G, Lombardo L, Bartolini S, Calandri C, de Rosa M, Villa E, Crino L. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2658-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860941&dopt=Abstract
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Gefitinib in recurrent non-small-cell lung cancer: an IDEAL trial? Author(s): Johnson DH, Arteaga CL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2227-9. Epub 2003 May 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748243&dopt=Abstract
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Gelatinolytic activity of matrix metalloproteinase in lung cancer studied using film in situ zymography stamp method. Author(s): Kaji M, Moriyama S, Sasaki H, Saitoh Y, Kiriyama M, Fukai I, Yamakawa Y, Mitsui A, Toyama T, Nemori R, Fujii Y. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 125-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581563&dopt=Abstract
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Gelsolin suppresses tumorigenicity through inhibiting PKC activation in a human lung cancer cell line, PC10. Author(s): Sagawa N, Fujita H, Banno Y, Nozawa Y, Katoh H, Kuzumaki N. Source: British Journal of Cancer. 2003 February 24; 88(4): 606-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592377&dopt=Abstract
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Gemcitabine (Gemzar)-based induction chemotherapy in non-small-cell lung cancer. Author(s): Scagliotti GV, Novello S. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38 Suppl 2: S13-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431824&dopt=Abstract
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Gemcitabine and carboplatin in patients with locally advanced or metastatic nonsmall cell lung cancer: a prospective phase II study. Author(s): Kortsik C, Albrecht P, Elmer A. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 85-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660012&dopt=Abstract
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Gemcitabine and cisplatin as induction chemotherapy for patients with unresectable Stage IIIA-bulky N2 and Stage IIIB nonsmall cell lung carcinoma: an Italian Lung Cancer Project Observational Study. Author(s): Cappuzzo F, Selvaggi G, Gregorc V, Mazzoni F, Betti M, Rita Migliorino M, Novello S, Maestri A, De Marinis F, Darwish S, De Angelis V, Nelli F, Bartolini S, Scagliotti GV, Tonato M, Crino L. Source: Cancer. 2003 July 1; 98(1): 128-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833465&dopt=Abstract
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Gemcitabine as single agent chemotherapy in elderly patients with stages III-IV nonsmall cell lung cancer (NSCLC): a phase II study. Author(s): Bianco V, Rozzi A, Tonini G, Santini D, Magnolfi E, Vincenzi B, D'Angelillo R, Marchei P. Source: Anticancer Res. 2002 September-October; 22(5): 3053-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530041&dopt=Abstract
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Gemcitabine in the treatment of advanced non-small cell lung cancer: report of one case. Author(s): Liu AH, Wang XS, Zhou Y, Duan EY, Wu YX. Source: Di Yi June Yi Da Xue Xue Bao. 2002 January; 22(1): 94-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390863&dopt=Abstract
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Gemcitabine plus cisplatin in the treatment of patients with advanced non-small cell lung cancer: a phase II study. Author(s): Bretti S, Manzin E, Loddo C, Berruti A, Bombaci S, Vellani G, Celano A. Source: Anticancer Res. 2002 September-October; 22(5): 3039-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530039&dopt=Abstract
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Gemcitabine/carboplatin in advanced non-small cell lung cancer. Author(s): Zatloukal P, Petruzelka L. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38 Suppl 2: S33-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431827&dopt=Abstract
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Gemzar platinum combinations: phase III trials in non-small cell lung cancer. Author(s): Crino L, Calandri C. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38 Suppl 2: S9-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431823&dopt=Abstract
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Gene and peptide analyses of newly defined lung cancer antigens recognized by HLA-A2402-restricted tumor-specific cytotoxic T lymphocytes. Author(s): Yamada A, Kawano K, Koga M, Takamori S, Nakagawa M, Itoh K. Source: Cancer Research. 2003 June 1; 63(11): 2829-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782588&dopt=Abstract
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Gene therapy for lung cancer. An introduction. Author(s): Haura EB, Sotomayor E, Antonia SJ. Source: Methods in Molecular Medicine. 2003; 75: 529-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407762&dopt=Abstract
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Gene-environment interactions between the codon 194 polymorphism of XRCC1 and antioxidants influence lung cancer risk. Author(s): Ratnasinghe DL, Yao SX, Forman M, Qiao YL, Andersen MR, Giffen CA, Erozan Y, Tockman MS, Taylor PR. Source: Anticancer Res. 2003 January-February; 23(1B): 627-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680158&dopt=Abstract
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Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer. Author(s): Osada H, Takahashi T. Source: Oncogene. 2002 October 21; 21(48): 7421-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12379883&dopt=Abstract
100 Lung Cancer
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Genetic alterations responsible for metastatic phenotypes of lung cancer cells. Author(s): Yokota J, Nishioka M, Tani M, Kohno T. Source: Clinical & Experimental Metastasis. 2003; 20(3): 189-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12741677&dopt=Abstract
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Genetic polymorphism of CYP2A6 gene and tobacco-induced lung cancer risk in male smokers. Author(s): Ariyoshi N, Miyamoto M, Umetsu Y, Kunitoh H, Dosaka-Akita H, Sawamura Y, Yokota J, Nemoto N, Sato K, Kamataki T. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 September; 11(9): 890-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12223434&dopt=Abstract
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Genetic polymorphisms and lung cancer susceptibility: a review. Author(s): Kiyohara C, Otsu A, Shirakawa T, Fukuda S, Hopkin JM. Source: Lung Cancer (Amsterdam, Netherlands). 2002 September; 37(3): 241-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234692&dopt=Abstract
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Genetic polymorphisms of glutathione S-transferases as modulators of lung cancer susceptibility. Author(s): Stucker I, Hirvonen A, de Waziers I, Cabelguenne A, Mitrunen K, Cenee S, Koum-Besson E, Hemon D, Beaune P, Loriot MA. Source: Carcinogenesis. 2002 September; 23(9): 1475-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12189190&dopt=Abstract
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Genetic susceptibility to lung cancer: implications for smoking cessation. Author(s): Houfek JF, Atwood JR. Source: Medsurg Nursing : Official Journal of the Academy of Medical-Surgical Nurses. 2003 February; 12(1): 45-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619599&dopt=Abstract
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Genetic testing for lung cancer risk: if physicians can do it, should they? Author(s): Marcy TW, Stefanek M, Thompson KM. Source: Journal of General Internal Medicine : Official Journal of the Society for Research and Education in Primary Care Internal Medicine. 2002 December; 17(12): 946-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472931&dopt=Abstract
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Geographical inequalities in lung cancer management and survival in South East England: evidence of variation in access to oncology services? Author(s): Jack RH, Gulliford MC, Ferguson J, Moller H. Source: British Journal of Cancer. 2003 April 7; 88(7): 1025-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671698&dopt=Abstract
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Glass-based radon-exposure assessment and lung cancer risk. Author(s): Lagarde F, Falk R, Almren K, Nyberg F, Svensson H, Pershagen G. Source: Journal of Exposure Analysis and Environmental Epidemiology. 2002 September; 12(5): 344-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12198583&dopt=Abstract
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Glucocorticoids inhibit lung cancer cell growth through both the extracellular signalrelated kinase pathway and cell cycle regulators. Author(s): Greenberg AK, Hu J, Basu S, Hay J, Reibman J, Yie TA, Tchou-Wong KM, Rom WN, Lee TC. Source: American Journal of Respiratory Cell and Molecular Biology. 2002 September; 27(3): 320-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12204894&dopt=Abstract
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Glutathione S-transferase M1 polymorphism and the risk of lung cancer. Author(s): Mohr LC, Rodgers JK, Silvestri GA. Source: Anticancer Res. 2003 May-June; 23(3A): 2111-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894585&dopt=Abstract
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Growth and molecular profile of lung cancer cells expressing ectopic LKB1: downregulation of the phosphatidylinositol 3'-phosphate kinase/PTEN pathway. Author(s): Jimenez AI, Fernandez P, Dominguez O, Dopazo A, Sanchez-Cespedes M. Source: Cancer Research. 2003 March 15; 63(6): 1382-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649203&dopt=Abstract
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GSTM1, GSTT1 and GSTP1 polymorphisms and lung cancer risk. Author(s): Lewis SJ, Cherry NM, Niven RM, Barber PV, Povey AC. Source: Cancer Letters. 2002 June 28; 180(2): 165-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12175548&dopt=Abstract
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Guidelines for the use of spiral computed tomography in screening for lung cancer. Author(s): Henschke CI, Yankelevitz DF, McCauley DI, Libby DM, Pasmantier MW, Smith JP. Source: Eur Respir J Suppl. 2003 January; 39: 45S-51S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572701&dopt=Abstract
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Guidelines on treatment of stage IIIB non-small cell lung cancer. Author(s): Jett JR, Scott WJ, Rivera MP, Sause WT; American College of Chest Physicians. Source: Chest. 2003 January; 123(1 Suppl): 221S-225S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527581&dopt=Abstract
102 Lung Cancer
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GVAX (GMCSF gene modified tumor vaccine) in advanced stage non small cell lung cancer. Author(s): Nemunaitis J. Source: Journal of Controlled Release : Official Journal of the Controlled Release Society. 2003 August 28; 91(1-2): 225-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932654&dopt=Abstract
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Has lung cancer in the elderly different characteristics at presentation? Author(s): Montella M, Gridelli C, Crispo A, Scognamiglio F, Ruffolo P, Gatani T, Boccia V, Maione P, Fabbrocini G. Source: Oncol Rep. 2002 September-October; 9(5): 1093-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12168079&dopt=Abstract
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Health perceptions and risk behaviors of lung cancer survivors. Author(s): Evangelista LS, Sarna L, Brecht ML, Padilla G, Chen J. Source: Heart & Lung : the Journal of Critical Care. 2003 March-April; 32(2): 131-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734536&dopt=Abstract
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Healthcare outcomes: gemcitabine cost-effectiveness in the treatment of non-small cell lung cancer. Author(s): Szczepura A. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38 Suppl 2: S21-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431825&dopt=Abstract
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Health-related quality of life in non-small-cell lung cancer: methodologic issues in randomized controlled trials. Author(s): Bottomley A, Efficace F, Thomas R, Vanvoorden V, Ahmedzai SH. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2982-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885819&dopt=Abstract
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Hedgehog signaling: progenitor phenotype in small-cell lung cancer. Author(s): Watkins DN, Berman DM, Baylin SB. Source: Cell Cycle (Georgetown, Tex.). 2003 May-June; 2(3): 196-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734424&dopt=Abstract
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Hedgehog signalling within airway epithelial progenitors and in small-cell lung cancer. Author(s): Watkins DN, Berman DM, Burkholder SG, Wang B, Beachy PA, Baylin SB. Source: Nature. 2003 March 20; 422(6929): 313-7. Epub 2003 Mar 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629553&dopt=Abstract
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Helical computed tomography for lung cancer screening. Author(s): Elwood M, Campbell DA, de Campo MP. Source: The Medical Journal of Australia. 2003 August 4; 179(3): 125-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885278&dopt=Abstract
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Hematogenous dissemination of lung cancer cells during surgery: quantitative detection by flow cytometry and prognostic significance. Author(s): Dong Q, Huang J, Zhou Y, Li L, Bao G, Feng J, Sha H. Source: Lung Cancer (Amsterdam, Netherlands). 2002 September; 37(3): 293-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234699&dopt=Abstract
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Hemoptysis as an unusual presenting symptom of invasion of a descending thoracic aortic aneurysmal dissection by lung cancer. Author(s): Tsui P, Lee JH, MacLennan G, Capdeville M. Source: Texas Heart Institute Journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital. 2002; 29(2): 136-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075873&dopt=Abstract
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High dose rate endobronchial brachytherapy effectively palliates symptoms due to inoperable lung cancer. Author(s): Celebioglu B, Gurkan OU, Erdogan S, Savas I, Kose K, Kurtman C, Gonullu U. Source: Japanese Journal of Clinical Oncology. 2002 November; 32(11): 443-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499415&dopt=Abstract
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High pretreatment serum concentration of basic fibroblast growth factor is a predictor of poor prognosis in small cell lung cancer. Author(s): Ruotsalainen T, Joensuu H, Mattson K, Salven P. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 November; 11(11): 1492-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12433733&dopt=Abstract
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High-dose chemotherapy in small cell lung cancer. Author(s): Pasini F, Pelosi G, De Manzoni G, Rosti G. Source: Tumori. 2002 May-June; 88(3): 179-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12195754&dopt=Abstract
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High-dose chemotherapy in small-cell lung cancer. Author(s): Pasini F, Durante E, De Manzoni D, Rosti G, Pelosi G. Source: Anticancer Res. 2002 November-December; 22(6B): 3465-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552940&dopt=Abstract
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High-dose conformal radiotherapy for treatment of stage IIIA/IIIB non-small-cell lung cancer: technical issues and results of a phase I/II trial. Author(s): Rosenman JG, Halle JS, Socinski MA, Deschesne K, Moore DT, Johnson H, Fraser R, Morris DE. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 October 1; 54(2): 348-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243807&dopt=Abstract
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HIV-related lung cancer in the era of highly active antiretroviral therapy. Author(s): Bower M, Powles T, Nelson M, Shah P, Cox S, Mandelia S, Gazzard B. Source: Aids (London, England). 2003 February 14; 17(3): 371-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556691&dopt=Abstract
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Hormonal factors and risk of lung cancer among women? Author(s): Kreuzer M, Gerken M, Heinrich J, Kreienbrock L, Wichmann HE. Source: International Journal of Epidemiology. 2003 April; 32(2): 263-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714547&dopt=Abstract
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How quality of life data contribute to our understanding of cancer patients' experiences? A study of patients with lung cancer. Author(s): Montazeri A, Milroy R, Hole D, McEwen J, Gillis CR. Source: Quality of Life Research : an International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 2003 March; 12(2): 157-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639062&dopt=Abstract
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How to optimize staging in early non-small cell lung cancer. Author(s): Jett JR. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): S13-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367808&dopt=Abstract
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HPV infections and lung cancer. Author(s): Syrjanen KJ. Source: Journal of Clinical Pathology. 2002 December; 55(12): 885-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461047&dopt=Abstract
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hTERT expression is a prognostic factor of survival in patients with stage I non-small cell lung cancer. Author(s): Wang L, Soria JC, Kemp BL, Liu DD, Mao L, Khuri FR. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 September; 8(9): 2883-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12231532&dopt=Abstract
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Hypermethylation of RASSF1A promoter is associated with the age at starting smoking and a poor prognosis in primary non-small cell lung cancer. Author(s): Kim DH, Kim JS, Ji YI, Shim YM, Kim H, Han J, Park J. Source: Cancer Research. 2003 July 1; 63(13): 3743-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839968&dopt=Abstract
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Hypoxia enhances the expression of plasminogen activator inhibitor-1 in human lung cancer cells, EBC-1. Author(s): Kimura D, Imaizumi T, Tamo W, Sakai T, Ito K, Hatanaka R, Yoshida H, Tsushima T, Satoh K, Fukuda I. Source: The Tohoku Journal of Experimental Medicine. 2002 April; 196(4): 259-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12086154&dopt=Abstract
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Identification of a novel homeobox-containing gene, LAGY, which is downregulated in lung cancer. Author(s): Chen Y, Petersen S, Pacyna-Gengelbach M, Pietas A, Petersen I. Source: Oncology. 2003; 64(4): 450-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759545&dopt=Abstract
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Identification of nuclear proteins of small cell lung cancer cell line H82: An improved procedure for the analysis of silver-stained proteins. Author(s): Gonzalez LJ, Castellanos-Serra L, Badock V, Diaz M, Moro A, Perea S, Santos A, Paz-Lago D, Otto A, Muller EC, Kostka S, Wittmann-Liebold B, Padron G. Source: Electrophoresis. 2003 January; 24(1-2): 237-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12652596&dopt=Abstract
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Identification of TDE2 gene and its expression in non-small cell lung cancer. Author(s): Player A, Gillespie J, Fujii T, Fukuoka J, Dracheva T, Meerzaman D, Hong KM, Curran J, Attoh G, Travis W, Jen J. Source: International Journal of Cancer. Journal International Du Cancer. 2003 November 1; 107(2): 238-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949800&dopt=Abstract
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Identification of tumor suppressor loci on the long arm of chromosome 15 in primary small cell lung cancer. Author(s): Kee HJ, Shin JH, Chang J, Chung KY, Shin DH, Kim YS, Kim SK, Kim SK. Source: Yonsei Medical Journal. 2003 February; 44(1): 65-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619177&dopt=Abstract
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Identifying patients at risk of early postoperative recurrence of lung cancer: a new use of the old CEA test. Author(s): Buccheri G, Ferrigno D. Source: The Annals of Thoracic Surgery. 2003 March; 75(3): 973-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645726&dopt=Abstract
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Immune cells in bronchoalveolar lavage in peripheral lung cancer--analysis of 140 cases. Author(s): Domagala-Kulawik J, Guzman J, Costabel U. Source: Respiration; International Review of Thoracic Diseases. 2003 January-February; 70(1): 43-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584390&dopt=Abstract
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Impact of treatment interruptions due to toxicity on outcome of patients with early stage (I/II) non-small-cell lung cancer (NSCLC) treated with hyperfractionated radiation therapy alone. Author(s): Jeremic B, Shibamoto Y, Milicic B, Dagovic A, Nikolic N, Aleksandrovic J, Acimovic L, Milisavljevic S. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 317-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781431&dopt=Abstract
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Impact of ZD1839 on non-small cell lung cancer-related symptoms as measured by the functional assessment of cancer therapy-lung scale. Author(s): Cella D. Source: Seminars in Oncology. 2003 February; 30(1 Suppl 1): 39-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644983&dopt=Abstract
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Improving surgical resection rates in lung cancer without a two stop service. Author(s): Bowen EF, Anderson JR, Roddie ME. Source: Thorax. 2003 April; 58(4): 368. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668811&dopt=Abstract
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In regard to Rosenman et al., high-dose conformal radiotherapy for treatment of stage III A/B non-small-cell lung cancer: technical issues and results of a phase I/II trial. IJROBP 2002;54:348-356. Author(s): Senan S, Lagerwaard FJ. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 April 1; 55(5): 1458-9; Author Reply 1459-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654460&dopt=Abstract
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In regard to Tsujino et al.: predictive value of dose-volume histogram parameters for predicting radiation pneumonitis after concurrent chemoradiation for lung cancer. IJROBP 2003;55:110-115. Author(s): Seppenwoolde Y, De Jaeger K, Lebesque JV. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 July 15; 56(4): 1208-9; Author Reply 1209. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829167&dopt=Abstract
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In vitro effects of combinations of cis-amminedichloro (2-methylpyridine) platinum (II) (ZD0473) with other novel anticancer drugs on the growth of SBC-3, a human small cell lung cancer cell line. Author(s): Kanzawa F, Akiyama Y, Saijo N, Nishio K. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 325-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781432&dopt=Abstract
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In vivo transglutaminase type 1 expression in normal lung, preinvasive bronchial lesions, and lung cancer. Author(s): Martinet N, Bonnard L, Regnault V, Picard E, Burke L, Siat J, Grosdidier G, Martinet Y, Vignaud JM. Source: American Journal of Respiratory Cell and Molecular Biology. 2003 April; 28(4): 428-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654631&dopt=Abstract
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Increased expression of the LGALS3 (galectin 3) gene in human non-small-cell lung cancer. Author(s): Yoshimura A, Gemma A, Hosoya Y, Komaki E, Hosomi Y, Okano T, Takenaka K, Matuda K, Seike M, Uematsu K, Hibino S, Shibuya M, Yamada T, Hirohashi S, Kudoh S. Source: Genes, Chromosomes & Cancer. 2003 June; 37(2): 159-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12696064&dopt=Abstract
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Independent predictive value of the overall number of metastatic N1 and N2 stations in lung cancer. Author(s): Ueda K, Kaneda Y, Sakano H, Tanaka T, Hayashi M, Li TS, Hamano K. Source: Jpn J Thorac Cardiovasc Surg. 2003 July; 51(7): 297-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892460&dopt=Abstract
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Independent prognostic value of fascin immunoreactivity in stage I nonsmall cell lung cancer. Author(s): Pelosi G, Pastorino U, Pasini F, Maissoneuve P, Fraggetta F, Iannucci A, Sonzogni A, De Manzoni G, Terzi A, Durante E, Bresaola E, Pezzella F, Viale G. Source: British Journal of Cancer. 2003 February 24; 88(4): 537-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592367&dopt=Abstract
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Individually different “weights” of quality of life assessment in patients with advanced nonsmall-cell lung cancer. Author(s): Morita S, Ohashi Y, Kobayashi K, Matsumoto T, Eguchi K, Shibuya M, Yamaji Y, Fukuoka M, Nagao K, Niitani H; West and East CPT-11 Lung Cancer Study Groups. Source: Journal of Clinical Epidemiology. 2003 August; 56(8): 744-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12954466&dopt=Abstract
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Induction chemotherapy in early-stage non-small-cell lung cancer. Author(s): Pisters KM. Source: Current Oncology Reports. 2003 July; 5(4): 307-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781072&dopt=Abstract
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Induction of apoptosis by combined treatment with differentiation-inducing agents and interferon-alpha in human lung cancer cells. Author(s): Yamamoto-Yamaguchi Y, Okabe-Kado J, Kasukabe T, Honma Y. Source: Anticancer Res. 2003 May-June; 23(3B): 2537-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894538&dopt=Abstract
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Inhibitors of epidermal-growth-factor receptors: a review of clinical research with a focus on non-small-cell lung cancer. Author(s): Sridhar SS, Seymour L, Shepherd FA. Source: The Lancet Oncology. 2003 July; 4(7): 397-406. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850190&dopt=Abstract
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Intentional limited pulmonary resection for peripheral T1 N0 M0 small-sized lung cancer. Author(s): Koike T, Yamato Y, Yoshiya K, Shimoyama T, Suzuki R. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 April; 125(4): 924-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12698157&dopt=Abstract
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Interleukin-10 expression is closely correlated with the expression of granulocytemacrophage colony-stimulating factor in non-small cell lung cancer. Author(s): Kamiya T, Hatanaka H, Abe Y, Kijima H, Yamazaki H, Ohnishi Y, Inoue H, Ueyama Y, Osamura Y, Nakamura M. Source: Anticancer Res. 2003 May-June; 23(3C): 2909-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926133&dopt=Abstract
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Intrathecal gemcitabine chemotherapy for non-small cell lung cancer patients with meningeal carcinomatosis--a case report. Author(s): Chen YM, Chen MC, Tsai CM, Perng RP. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 99-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660014&dopt=Abstract
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Intrathoracic staging in non small cell lung cancer: re-do mediastinoscopy revisited. Author(s): Cesario A, Margaritora S, Porziella V, Granone P, Trodella L, D'Angelillo RM. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 227-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711126&dopt=Abstract
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Investigation of anticancer mechanism of thiadiazole-based compound in human non-small cell lung cancer A549 cells. Author(s): Chou JY, Lai SY, Pan SL, Jow GM, Chern JW, Guh JH. Source: Biochemical Pharmacology. 2003 July 1; 66(1): 115-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818371&dopt=Abstract
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JAMA patient page. Lung cancer. Author(s): Parmet S, Lynm C, Glass RM. Source: Jama : the Journal of the American Medical Association. 2003 January 15; 289(3): 380. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532974&dopt=Abstract
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Joint action of smoking and asbestos exposure on lung cancer. Author(s): Liddell FD. Source: Occupational and Environmental Medicine. 2002 July; 59(7): 494-5; Author Reply 495-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12107302&dopt=Abstract
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Joint effects of radiation and smoking on lung cancer risk among atomic bomb survivors. Author(s): Pierce DA, Sharp GB, Mabuchi K. Source: Radiation Research. 2003 April; 159(4): 511-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643796&dopt=Abstract
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Kaempferol-induced growth inhibition and apoptosis in A549 lung cancer cells is mediated by activation of MEK-MAPK. Author(s): Nguyen TT, Tran E, Ong CK, Lee SK, Do PT, Huynh TT, Nguyen TH, Lee JJ, Tan Y, Ong CS, Huynh H. Source: Journal of Cellular Physiology. 2003 October; 197(1): 110-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942547&dopt=Abstract
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Ki-67 expression and prognosis for smokers with resected stage I non-small cell lung cancer. Author(s): Haga Y, Hiroshima K, Iyoda A, Shibuya K, Shimamura F, Iizasa T, Fujisawa T, Ohwada H. Source: The Annals of Thoracic Surgery. 2003 June; 75(6): 1727-32; Discussion 1732-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822607&dopt=Abstract
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L523S, an RNA-binding protein as a potential therapeutic target for lung cancer. Author(s): Wang T, Fan L, Watanabe Y, McNeill PD, Moulton GG, Bangur C, Fanger GR, Okada M, Inoue Y, Persing DH, Reed SG. Source: British Journal of Cancer. 2003 March 24; 88(6): 887-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644826&dopt=Abstract
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Lack of evidence for a role of Epstein-Barr virus in the increase of lung cancer in idiopathic pulmonary fibrosis. Author(s): Hayakawa H, Shirai M, Uchiyama H, Imokawa S, Suda T, Chida K, Muro H. Source: Respiratory Medicine. 2003 March; 97(3): 281-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645836&dopt=Abstract
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Lactate dehydrogenase-5 (LDH-5) overexpression in non-small-cell lung cancer tissues is linked to tumour hypoxia, angiogenic factor production and poor prognosis. Author(s): Koukourakis MI, Giatromanolaki A, Sivridis E, Bougioukas G, Didilis V, Gatter KC, Harris AL; Tumour and Angiogenesis Research Group. Source: British Journal of Cancer. 2003 September 1; 89(5): 877-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942121&dopt=Abstract
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Liver metastases from lung cancer: is surgical resection justified? Author(s): Di Carlo I, Grasso G, Patane' D, Russello D, Latteri F. Source: The Annals of Thoracic Surgery. 2003 July; 76(1): 291-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842567&dopt=Abstract
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Liver metastasis at the time of initial diagnosis of lung cancer. Author(s): Kagohashi K, Satoh H, Ishikawa H, Ohtsuka M, Sekizawa K. Source: Medical Oncology (Northwood, London, England). 2003; 20(1): 25-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665681&dopt=Abstract
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Long-term changes in pulmonary function tests after definitive radiotherapy for lung cancer. Author(s): Miller KL, Zhou SM, Barrier RC Jr, Shafman T, Folz RJ, Clough RW, Marks LB. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 July 1; 56(3): 611-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788165&dopt=Abstract
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Loss of heterozygosity on the long arm of chromosome 21 in non-small cell lung cancer. Author(s): Lee EB, Park TI, Park SH, Park JY. Source: The Annals of Thoracic Surgery. 2003 May; 75(5): 1597-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735585&dopt=Abstract
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Loss of PDCD4 expression in human lung cancer correlates with tumour progression and prognosis. Author(s): Chen Y, Knosel T, Kristiansen G, Pietas A, Garber ME, Matsuhashi S, Ozaki I, Petersen I. Source: The Journal of Pathology. 2003 August; 200(5): 640-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898601&dopt=Abstract
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Low lung function and incident lung cancer in the United States: data From the First National Health and Nutrition Examination Survey follow-up. Author(s): Mannino DM, Aguayo SM, Petty TL, Redd SC. Source: Archives of Internal Medicine. 2003 June 23; 163(12): 1475-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824098&dopt=Abstract
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Lung cancer * 8: Management of malignant mesothelioma. Author(s): Parker C, Neville E. Source: Thorax. 2003 September; 58(9): 809-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947146&dopt=Abstract
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Lung cancer 5: state of the art radiotherapy for lung cancer. Author(s): Price A. Source: Thorax. 2003 May; 58(5): 447-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728171&dopt=Abstract
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Lung cancer 7: management of lung cancer in elderly patients. Author(s): Booton R, Jones M, Thatcher N. Source: Thorax. 2003 August; 58(8): 711-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885992&dopt=Abstract
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Lung cancer and related risk factors: an update of the literature. Author(s): Ruano-Ravina A, Figueiras A, Barros-Dios JM. Source: Public Health. 2003 May; 117(3): 149-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825464&dopt=Abstract
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Lung cancer and Rosai-Dorfman's disease. A clinicopathological study. Author(s): Lutterbach J, Henne K, Pagenstecher A, Bohm J. Source: Strahlentherapie Und Onkologie : Organ Der Deutschen Rontgengesellschaft. [et Al]. 2003 July; 179(7): 486-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835886&dopt=Abstract
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Lung cancer associated with diffuse pulmonary fibrosis: CT-pathologic correlation. Author(s): Sakai S, Ono M, Nishio T, Kawarada Y, Nagashima A, Toyoshima S. Source: Journal of Thoracic Imaging. 2003 April; 18(2): 67-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12700479&dopt=Abstract
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Lung cancer associated with sarcoidosis. Author(s): Sato Y, Sasano S, Oyama K, Sakuraba M, Onuki T, Nitta S. Source: Jpn J Thorac Cardiovasc Surg. 2003 January; 51(1): 21-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645151&dopt=Abstract
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Lung cancer in elderly patients. Author(s): Hey JC. Source: Clinics in Geriatric Medicine. 2003 February; 19(1): 139-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735119&dopt=Abstract
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Lung cancer in heavy equipment operators and truck drivers with diesel exhaust exposure in the construction industry. Author(s): Jarvholm B, Silverman D. Source: Occupational and Environmental Medicine. 2003 July; 60(7): 516-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819286&dopt=Abstract
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Lung cancer incidence among Norwegian nickel-refinery workers 1953-2000. Author(s): Grimsrud TK, Berge SR, Martinsen JI, Andersen A. Source: Journal of Environmental Monitoring : Jem. 2003 April; 5(2): 190-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729252&dopt=Abstract
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Lung cancer mortality among chromate production workers. Author(s): Luippold RS, Mundt KA, Austin RP, Liebig E, Panko J, Crump C, Crump K, Proctor D. Source: Occupational and Environmental Medicine. 2003 June; 60(6): 451-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771398&dopt=Abstract
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Lung cancer patterns of care in south western Sydney, Australia. Author(s): Vinod SK, Delaney GP, Bauman AE, Barton MB. Source: Thorax. 2003 August; 58(8): 690-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885986&dopt=Abstract
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Lung cancer risk in germline p53 mutation carriers: association between an inherited cancer predisposition, cigarette smoking, and cancer risk. Author(s): Hwang SJ, Cheng LS, Lozano G, Amos CI, Gu X, Strong LC. Source: Human Genetics. 2003 August; 113(3): 238-43. Epub 2003 June 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802680&dopt=Abstract
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Lung cancer risk in white and black Americans. Author(s): Stellman SD, Chen Y, Muscat JE, Djordjevic MV, Richie JP Jr, Lazarus P, Thompson S, Altorki N, Berwick M, Citron ML, Harlap S, Kaur TB, Neugut AI, Olson S, Travaline JM, Witorsch P, Zhang ZF. Source: Annals of Epidemiology. 2003 April; 13(4): 294-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684197&dopt=Abstract
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Lung cancer risk in workers exposed to poly(vinyl chloride) dust: a nested casereferent study. Author(s): Mastrangelo G, Fedeli U, Fadda E, Milan G, Turato A, Pavanello S. Source: Occupational and Environmental Medicine. 2003 June; 60(6): 423-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771394&dopt=Abstract
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Lung cancer screening with low-dose computed tomography. Author(s): Hartman TE, Swensen SJ. Source: Semin Roentgenol. 2003 January; 38(1): 34-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12698589&dopt=Abstract
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Lung cancer screening. Author(s): Truong MT, Munden RF. Source: Current Oncology Reports. 2003 July; 5(4): 309-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781073&dopt=Abstract
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Lung cancer treatment present and future. Author(s): Cho JK. Source: Hawaii Med J. 2003 March; 62(3): 61-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703177&dopt=Abstract
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Lung cancer. 6: The case for limited surgical resection in non-small cell lung cancer. Author(s): Sugarbaker DJ. Source: Thorax. 2003 July; 58(7): 639-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12832686&dopt=Abstract
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Lung cancer. 9: Molecular biology of lung cancer: clinical implications. Author(s): Fong KM, Sekido Y, Gazdar AF, Minna JD. Source: Thorax. 2003 October; 58(10): 892-900. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514947&dopt=Abstract
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Lung cancer: the importance of seeing a respiratory physician. Author(s): Fergusson RJ, Thomson CS, Brewster DH, Brown PH, Milroy R; Scottish Cancer Trials Lung Group; Scottish Cancer Therapy Network. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 April; 21(4): 606-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762343&dopt=Abstract
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Macrophage migration inhibitory factor and CXC chemokine expression in non-small cell lung cancer: role in angiogenesis and prognosis. Author(s): White ES, Flaherty KR, Carskadon S, Brant A, Iannettoni MD, Yee J, Orringer MB, Arenberg DA. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 February; 9(2): 853-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576459&dopt=Abstract
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Major conceptual change required to improve lung cancer: see a respiratory physician. Author(s): Field JK, Brambilla C. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 April; 21(4): 565-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762336&dopt=Abstract
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MALAT-1, a novel noncoding RNA, and thymosin beta4 predict metastasis and survival in early-stage non-small cell lung cancer. Author(s): Ji P, Diederichs S, Wang W, Boing S, Metzger R, Schneider PM, Tidow N, Brandt B, Buerger H, Bulk E, Thomas M, Berdel WE, Serve H, Muller-Tidow C. Source: Oncogene. 2003 September 11; 22(39): 6087-97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970751&dopt=Abstract
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Malignant status at surgical margin of limited-resected non-small cell lung cancer: a crucial finding for predicting local relapse. Author(s): Sawabata N. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 August; 126(2): 610-1; Author Reply 611. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928675&dopt=Abstract
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Management for chest wall implantation of non-small cell lung cancer after fineneedle aspiration biopsy. Author(s): Kim JH, Kim YT, Lim HK, Kim YH, Sung SW. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 May; 23(5): 828-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754041&dopt=Abstract
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Management of the irradiated bronchus after lobectomy for lung cancer. Author(s): Greason KL, Miller DL, Clay RP, Deschamps C, Johnson CH, Allen MS, Trastek VF, Pairolero PC. Source: The Annals of Thoracic Surgery. 2003 July; 76(1): 180-5; Discussion 185-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842536&dopt=Abstract
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MDR-1 C3435T genetic polymorphism and tobacco-related lung cancer. Author(s): Sinues B, Fanlo A, Bernal ML, Mayayo E, Bello S, Rubio E, Isla D. Source: Oncology. 2003; 64(2): 183-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566917&dopt=Abstract
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Measurement of chemoresistance markers in patients with stage III non-small cell lung cancer: a novel approach for patient selection. Author(s): Brooks KR, To K, Joshi MB, Conlon DH, Herndon JE 2nd, D'Amico TA, Harpole DH Jr. Source: The Annals of Thoracic Surgery. 2003 July; 76(1): 187-93; Discussion 193. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842538&dopt=Abstract
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Mechanisms of metastasis as related to receptor tyrosine kinases in small-cell lung cancer. Author(s): Jafri NF, Ma PC, Maulik G, Salgia R. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 2003; 22(3): 14765. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14529091&dopt=Abstract
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Mechanisms of proteasome inhibitor PS-341-induced G(2)-M-phase arrest and apoptosis in human non-small cell lung cancer cell lines. Author(s): Ling YH, Liebes L, Jiang JD, Holland JF, Elliott PJ, Adams J, Muggia FM, Perez-Soler R. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 March; 9(3): 1145-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631620&dopt=Abstract
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Mediastinoscopy in patients with clinical stage I non-small cell lung cancer. Author(s): Choi YS, Shim YM, Kim J, Kim K. Source: The Annals of Thoracic Surgery. 2003 February; 75(2): 364-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12607640&dopt=Abstract
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Menstrual and reproductive factors and risk of lung cancer among Chinese women, Eastern Gansu Province, 1994-1998. Author(s): Brenner AV, Wang Z, Kleinerman RA, Lei S, Metayer C, Wang W, Lubin JH. Source: J Epidemiol. 2003 January; 13(1): 22-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587610&dopt=Abstract
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Menthol cigarettes and risk of lung cancer. Author(s): Brooks DR, Palmer JR, Strom BL, Rosenberg L. Source: American Journal of Epidemiology. 2003 October 1; 158(7): 609-16; Discussion 617-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507595&dopt=Abstract
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Metastatic lung cancer in pregnancy. Author(s): Wong CM, Lim KH, Liam CK. Source: Respirology (Carlton, Vic.). 2003 March; 8(1): 107-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856752&dopt=Abstract
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Methylation patterns and K-ras mutations in tumor and paired serum of resected nonsmall-cell lung cancer patients. Author(s): Ramirez JL, Sarries C, de Castro PL, Roig B, Queralt C, Escuin D, de Aguirre I, Sanchez JM, Manzano JL, Margeli M, Sanchez JJ, Astudillo J, Taron M, Rosell R. Source: Cancer Letters. 2003 April 25; 193(2): 207-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706879&dopt=Abstract
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Minimal alteration of pulmonary function after lobectomy in lung cancer patients with chronic obstructive pulmonary disease. Author(s): Sekine Y, Iwata T, Chiyo M, Yasufuku K, Motohashi S, Yoshida S, Suzuki M, Iizasa T, Saitoh Y, Fujisawa T. Source: The Annals of Thoracic Surgery. 2003 August; 76(2): 356-61; Discussion 362. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902063&dopt=Abstract
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Mitochondrial DNA mutation correlates with stage progression and prognosis in non-small cell lung cancer. Author(s): Matsuyama W, Nakagawa M, Wakimoto J, Hirotsu Y, Kawabata M, Osame M. Source: Human Mutation. 2003 April; 21(4): 441-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655558&dopt=Abstract
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Molecular and cellular biology of small cell lung cancer. Author(s): Sattler M, Salgia R. Source: Seminars in Oncology. 2003 February; 30(1): 57-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635090&dopt=Abstract
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Monocyte-derived microparticles may be a sign of vascular complication in patients with lung cancer. Author(s): Kanazawa S, Nomura S, Kuwana M, Muramatsu M, Yamaguchi K, Fukuhara S. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 145-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581566&dopt=Abstract
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Mortality due to silico-tuberculosis and lung cancer among 200 whetstone cutters. Author(s): Ogawa S, Imai H, Ikeda M. Source: Ind Health. 2003 July; 41(3): 231-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12916753&dopt=Abstract
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Mortality trend of lung cancer in Japan: 1960-2000. Author(s): Marugame T, Mizuno S. Source: Japanese Journal of Clinical Oncology. 2003 March; 33(3): 148-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710458&dopt=Abstract
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Multidetector-row CT of lung cancer screening. Author(s): Jacobson FL. Source: Semin Roentgenol. 2003 April; 38(2): 168-75. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854440&dopt=Abstract
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Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer. Author(s): Fukuoka M, Yano S, Giaccone G, Tamura T, Nakagawa K, Douillard JY, Nishiwaki Y, Vansteenkiste J, Kudoh S, Rischin D, Eek R, Horai T, Noda K, Takata I, Smit E, Averbuch S, Macleod A, Feyereislova A, Dong RP, Baselga J. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2237-46. Epub 2003 May 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12748244&dopt=Abstract
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Multi-slice/helical computed tomography for lung cancer screening. Author(s): Banerjee S. Source: Issues Emerg Health Technol. 2003 June; (48): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12812212&dopt=Abstract
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Mutational analysis of the transforming growth factor beta receptor type I gene in primary non-small cell lung cancer. Author(s): Zhang HT, Fei QY, Chen F, Qi QY, Zou W, Wang JC, Zhang RM, Tao SH, Chen XF, Luo ZW. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 281-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781426&dopt=Abstract
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Negative aspects of preoperative delay in early stage non-small cell lung cancer. Author(s): Sortini A, Sortini D, Carrella G. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 August; 126(2): 60910; Author Reply 610. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928674&dopt=Abstract
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Neoadjuvant and adjuvant therapy of non-small cell lung cancer. Author(s): Rajdev L, Keller SM. Source: Surgical Oncology. 2002 December; 11(4): 243-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450560&dopt=Abstract
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Neoadjuvant chemotherapy and chemoradiotherapy for non-small cell lung cancer: current status and future prospects. Author(s): Edelman MJ. Source: Expert Opinion on Pharmacotherapy. 2003 June; 4(6): 843-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783581&dopt=Abstract
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Neoadjuvant chemotherapy with gemcitabine and cisplatin in stage IIIA/B non-small cell lung cancer. Author(s): Van Kooten M, Rosenberg M, Orlando M, Morero J, Vilanova M, Rojas O, Vicente H, Bagnes C, Silva C, Chacon RD. Source: Investigational New Drugs. 2002 November; 20(4): 439-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448663&dopt=Abstract
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Neural-cadherin expression associated with angiogenesis in non-small-cell lung cancer patients. Author(s): Nakashima T, Huang C, Liu D, Kameyama K, Masuya D, Kobayashi S, Kinoshita M, Yokomise H. Source: British Journal of Cancer. 2003 June 2; 88(11): 1727-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771988&dopt=Abstract
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Neuroendocrine alterations in lung cancer patients. Author(s): Mazzoccoli G, Carughi S, De Cata A, La Viola M, Giuliani A, Tarquini R, Perfetto F. Source: Neuroendocrinol Lett. 2003 February-April; 24(1-2): 77-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743538&dopt=Abstract
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Neuroendocrine and cytokeratin serum markers as prognostic determinants of small cell lung cancer. Author(s): Pujol JL, Quantin X, Jacot W, Boher JM, Grenier J, Lamy PJ. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 131-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581564&dopt=Abstract
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New approaches for biomarker discovery in lung cancer. Author(s): Valle RP, Chavany C, Zhukov TA, Jendoubi M. Source: Expert Rev Mol Diagn. 2003 January; 3(1): 55-67. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528364&dopt=Abstract
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New approaches in the treatment of non-small cell lung cancer: taxanes in the treatment of NSCLC: pathways to progress. Author(s): Kris MG, Tonato M. Source: Lung Cancer (Amsterdam, Netherlands). 2002 December; 38 Suppl 4: 1-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480188&dopt=Abstract
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New model predicts risk of developing lung cancer. Author(s): Rollins G. Source: Rep Med Guidel Outcomes Res. 2003 April 18; 14(8): 9-10, 12. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854531&dopt=Abstract
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New potentials of radiotherapy in non-small cell lung cancer: stereotactic therapy and IMRT. Author(s): Van Houtte P. Source: Current Problems in Cancer. 2003 January-February; 27(1): 60-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569353&dopt=Abstract
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New prognostic indicator for non-small-cell lung cancer, quantitation of thymidylate synthase by real-time reverse transcription polymerase chain reaction. Author(s): Shintani Y, Ohta M, Hirabayashi H, Tanaka H, Iuchi K, Nakagawa K, Maeda H, Kido T, Miyoshi S, Matsuda H. Source: International Journal of Cancer. Journal International Du Cancer. 2003 May 10; 104(6): 790-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640689&dopt=Abstract
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New targeted therapies for lung cancer: expectations and reality. Author(s): Bunn PA Jr. Source: Medgenmed [electronic Resource] : Medscape General Medicine. 2002 August 5; 4(3): 12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466755&dopt=Abstract
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New targets for the treatment of advanced non-small cell lung cancer. Author(s): Massarelli E, Onn A, Zinner R, Khuri FR, Kim ES, Herbst RS. Source: Cancer Chemother Biol Response Modif. 2002; 20: 717-61. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703232&dopt=Abstract
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New techniques for early detection of lung cancer. Author(s): Sutedja G. Source: Eur Respir J Suppl. 2003 January; 39: 57S-66S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572703&dopt=Abstract
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Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. Author(s): Minna JD. Source: The Journal of Clinical Investigation. 2003 January; 111(1): 31-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12511585&dopt=Abstract
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No association between the p21 codon 31 serine-arginine polymorphism and lung cancer risk. Author(s): Su L, Liu G, Zhou W, Xu LL, Miller DP, Park S, Lynch TJ, Wain JC, Christiani DC. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2003 February; 12(2): 174-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582031&dopt=Abstract
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Noninvasive staging of non-small cell lung cancer: a review of the current evidence. Author(s): Toloza EM, Harpole L, McCrory DC. Source: Chest. 2003 January; 123(1 Suppl): 137S-146S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527573&dopt=Abstract
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Nonradioactive iodide effectively induces apoptosis in genetically modified lung cancer cells. Author(s): Zhang L, Sharma S, Zhu LX, Kogai T, Hershman JM, Brent GA, Dubinett SM, Huang M. Source: Cancer Research. 2003 August 15; 63(16): 5065-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941836&dopt=Abstract
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Non-small cell lung cancer staging techniques and endoscopic ultrasound: tissue is still the issue. Author(s): LeBlanc JK, Espada R, Ergun G. Source: Chest. 2003 May; 123(5): 1718-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740292&dopt=Abstract
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Non-small cell lung cancer with chest wall invasion: evolution of surgical treatment and prognosis in the last 3 decades. Author(s): Roviaro G, Varoli F, Grignani F, Vergani C, Pagano C, Maciocco M, Romanelli A. Source: Chest. 2003 May; 123(5): 1341-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740245&dopt=Abstract
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Non-small cell lung cancer with chest wall involvement. Author(s): Karmy-Jones R, Vallieres E. Source: Chest. 2003 May; 123(5): 1323-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740237&dopt=Abstract
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Non-small cell lung cancer-derived soluble mediators enhance apoptosis in activated T lymphocytes through an I kappa B kinase-dependent mechanism. Author(s): Batra RK, Lin Y, Sharma S, Dohadwala M, Luo J, Pold M, Dubinett SM. Source: Cancer Research. 2003 February 1; 63(3): 642-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566308&dopt=Abstract
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Novel therapies for lung cancer. Author(s): Hoang T, Traynor AM, Schiller JH. Source: Surgical Oncology. 2002 December; 11(4): 229-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450559&dopt=Abstract
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Novel therapies for the treatment of non-small cell lung cancer. Author(s): Johnson DH, Schiller JH. Source: Cancer Chemother Biol Response Modif. 2002; 20: 763-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703233&dopt=Abstract
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Nuclear accumulation of p53 is a potential marker for the development of squamous cell lung cancer in smokers. Author(s): Piyathilake CJ, Frost AR, Manne U, Weiss H, Heimburger DC, Grizzle WE. Source: Chest. 2003 January; 123(1): 181-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527620&dopt=Abstract
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Nurse led follow up and conventional medical follow up in management of patients with lung cancer: randomised trial. Author(s): Moore S, Corner J, Haviland J, Wells M, Salmon E, Normand C, Brada M, O'Brien M, Smith I. Source: Bmj (Clinical Research Ed.). 2002 November 16; 325(7373): 1145. Erratum In: Bmj 2002 December 14; 325(7377): 1386. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12433764&dopt=Abstract
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Nurse practitioners' knowledge, practice and attitudes about tobacco cessation & lung cancer screening. Author(s): Lawvere S, Mahoney MC, Englert JJ, Murphy JM, Hyland A, Klein SB, Loewen GM. Source: Journal of the American Academy of Nurse Practitioners. 2003 August; 15(8): 376-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509103&dopt=Abstract
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Nursing assessment and management of dyspneic patients with lung cancer. Author(s): Inzeo D, Tyson L. Source: Clinical Journal of Oncology Nursing. 2003 May-June; 7(3): 332-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793341&dopt=Abstract
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Oat cell lung cancer diagnosed following metastasis to the skin. Author(s): Senen D, Adanali G, Tuncel A, Erdogan B. Source: Plastic and Reconstructive Surgery. 2003 January; 111(1): 510-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496648&dopt=Abstract
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Observation-only management of inoperable lung cancer: do not do that: a loud and clear radiographic point of view! Author(s): Jeremic B, Classen J, Bamberg M. Source: Chest. 2003 January; 123(1): 313-4; Author Reply 314-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527646&dopt=Abstract
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Occupation and smoking as risk factors for lung cancer: a population-based casecontrol study. Author(s): Ruano-Ravina A, Figueiras A, Barreiro-Carracedo MA, Barros-Dios J. Source: American Journal of Industrial Medicine. 2003 February; 43(2): 149-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12541269&dopt=Abstract
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Occupational exposures and lung cancer in New Caledonia. Author(s): Menvielle G, Luce D, Fevotte J, Bugel I, Salomon C, Goldberg P, BillonGalland MA, Goldberg M. Source: Occupational and Environmental Medicine. 2003 August; 60(8): 584-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12883019&dopt=Abstract
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Older people with non small cell lung cancer in clinical stage IIIA and co-morbid conditions. Is curative irradiation feasible? Final results of a prospective study. Author(s): Pergolizzi S, Santacaterina A, Renzis CD, Settineri N, Gaeta M, Frosina P, Russi EG, Altavilla G. Source: Lung Cancer (Amsterdam, Netherlands). 2002 August; 37(2): 201-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140143&dopt=Abstract
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On the origin of G --> T transversions in lung cancer. Author(s): Pfeifer GP, Hainaut P. Source: Mutation Research. 2003 May 15; 526(1-2): 39-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714181&dopt=Abstract
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One from column A: choosing between CT, positron emission tomography, endoscopic ultrasound with fine-needle aspiration, transbronchial needle aspiration, thoracoscopy, mediastinoscopy, and mediastinotomy for staging lung cancer. Author(s): Silvestri GA, Hoffman B, Reed CE. Source: Chest. 2003 February; 123(2): 333-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576346&dopt=Abstract
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ONS participates in American College of Chest Physicians Lung Cancer Guidelines Project. Author(s): Cooley ME. Source: Ons News / Oncology Nursing Society. 2003 January; 18(1): 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12599863&dopt=Abstract
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Organ heterogeneity of host-derived matrix metalloproteinase expression and its involvement in multiple-organ metastasis by lung cancer cell lines. Author(s): Shiraga M, Yano S, Yamamoto A, Ogawa H, Goto H, Miki T, Miki K, Zhang H, Sone S. Source: Cancer Research. 2002 October 15; 62(20): 5967-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12384564&dopt=Abstract
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Outcome and prognostic factors for patients with non-small-cell lung cancer and severe radiation pneumonitis. Author(s): Wang JY, Chen KY, Wang JT, Chen JH, Lin JW, Wang HC, Lee LN, Yang PC. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 November 1; 54(3): 735-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377325&dopt=Abstract
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Outcome in patients with lung cancer found on lung cancer mass screening roentgenograms, but who did not subsequently consult a doctor. Author(s): Kashiwabara K, Koshi S, Itonaga K, Nakahara O, Tanaka M, Toyonaga M. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 67-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660008&dopt=Abstract
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Outcome of patients admitted to the intensive care unit with newly diagnosed small cell lung cancer. Author(s): Jennens RR, Rosenthal MA, Mitchell P, Presneill JJ. Source: Lung Cancer (Amsterdam, Netherlands). 2002 December; 38(3): 291-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12445751&dopt=Abstract
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Overexpression of CCR7 mRNA in nonsmall cell lung cancer: correlation with lymph node metastasis. Author(s): Takanami I. Source: International Journal of Cancer. Journal International Du Cancer. 2003 June 10; 105(2): 186-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673677&dopt=Abstract
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Overexpression of WISP-1 down-regulated motility and invasion of lung cancer cells through inhibition of Rac activation. Author(s): Soon LL, Yie TA, Shvarts A, Levine AJ, Su F, Tchou-Wong KM. Source: The Journal of Biological Chemistry. 2003 March 28; 278(13): 11465-70. Epub 2003 January 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529380&dopt=Abstract
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Overview of clinical trials with epidermal growth factor receptor inhibitors in advanced non-small cell lung cancer. Author(s): Thomas M. Source: Semin Oncol Nurs. 2002 November; 18(4 Suppl 4): 20-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534150&dopt=Abstract
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Overview of methodology for lung cancer evidence review and guideline development. Author(s): McCrory DC, Colice GL, Lewis SZ, Alberts WM, Parker S. Source: Chest. 2003 January; 123(1 Suppl): 3S-6S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527561&dopt=Abstract
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p53 gene mutations in non-small cell lung cancer detected by polymerase chain reaction single-strand conformation polymorphism analysis. Author(s): Zhao Y, Wu D, Xiang X, Zhang B, Zhou N, Hu Y. Source: Chinese Medical Sciences Journal = Chung-Kuo I Hsueh K'o Hsueh Tsa Chih / Chinese Academy of Medical Sciences. 1999 September; 14(3): 134-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12903811&dopt=Abstract
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p53 mutations and survival in stage I non-small-cell lung cancer: results of a prospective study. Author(s): Ahrendt SA, Hu Y, Buta M, McDermott MP, Benoit N, Yang SC, Wu L, Sidransky D. Source: Journal of the National Cancer Institute. 2003 July 2; 95(13): 961-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837832&dopt=Abstract
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Paraneoplastic sensory neuronopathy and spontaneous regression of small cell lung cancer. Author(s): Gill S, Murray N, Dalmau J, Thiessen B. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 2003 August; 30(3): 269-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12945955&dopt=Abstract
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Persistent excess mortality from lung cancer in patients with stage I non-small-cell lung cancer, disease-free after 5 years. Author(s): Pasini F, Verlato G, Durante E, de Manzoni G, Valduga F, Accordini S, Pedrazzani C, Terzi A, Pelosi G. Source: British Journal of Cancer. 2003 June 2; 88(11): 1666-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771977&dopt=Abstract
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Phase I trial of fixed dose-rate gemcitabine in combination with carboplatin in chemonaive advanced non-small-cell lung cancer: a Cancer Therapeutics Research Group study. Author(s): Soo RA, Lim HL, Wang LZ, Lee HS, Millward MJ, Tok LT, Lee SC, Lehnert M, Goh BC. Source: Cancer Chemotherapy and Pharmacology. 2003 August; 52(2): 153-8. Epub 2003 May 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750842&dopt=Abstract
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Phase I/II study of daily carboplatin, 5-fluorouracil and concurrent radiation therapy for locally advanced non-small-cell lung cancer. Author(s): Yoshizawa H, Tanaka J, Kagamu H, Maruyama Y, Miyao H, Ito K, Sato T, Iwashima A, Suzuki E, Gejyo F. Source: British Journal of Cancer. 2003 September 1; 89(5): 803-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942108&dopt=Abstract
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Physical activity and the risk of lung cancer in Canada. Author(s): Mao Y, Pan S, Wen SW, Johnson KC; Canadian Cancer Registries Epidemiology Research Group. Source: American Journal of Epidemiology. 2003 September 15; 158(6): 564-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965882&dopt=Abstract
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Pooled analysis of the CYP1A1 exon 7 polymorphism and lung cancer (United States). Author(s): Le Marchand L, Guo C, Benhamou S, Bouchardy C, Cascorbi I, Clapper ML, Garte S, Haugen A, Ingelman-Sundberg M, Kihara M, Rannug A, Ryberg D, Stucker I, Sugimura H, Taioli E. Source: Cancer Causes & Control : Ccc. 2003 May; 14(4): 339-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846365&dopt=Abstract
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Population- and community-based recruitment of African Americans and Latinos: the San Francisco Bay Area Lung Cancer Study. Author(s): Cabral DN, Napoles-Springer AM, Miike R, McMillan A, Sison JD, Wrensch MR, Perez-Stable EJ, Wiencke JK; San Francisco Bay Area Lung Cancer Study. Source: American Journal of Epidemiology. 2003 August 1; 158(3): 272-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882950&dopt=Abstract
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Positive reactions for both Cyfra21-1 and CA125 indicate worst prognosis in nonsmall cell lung cancer. Author(s): Ando S, Kimura H, Iwai N, Yamamoto N, Iida T. Source: Anticancer Res. 2003 May-June; 23(3C): 2869-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926125&dopt=Abstract
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Products of oxidative DNA damage and repair as possible biomarkers of susceptibility to lung cancer. Author(s): Gackowski D, Speina E, Zielinska M, Kowalewski J, Rozalski R, Siomek A, Paciorek T, Tudek B, Olinski R. Source: Cancer Research. 2003 August 15; 63(16): 4899-902. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941813&dopt=Abstract
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Prognostic factors for the survival of surgically treated patients for non-small cell lung cancer. Author(s): Fernandes OJ, Almgren SO, Thaning L, Filbey D, Helsing M, Karlsson M, Magnusson A, Souza D. Source: Acta Oncologica (Stockholm, Sweden). 2003; 42(4): 338-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899506&dopt=Abstract
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Prognostic significance of bcl-2 expression in resected pN2 non-small cell lung cancer. Author(s): Tomita M, Matsuzaki Y, Edagawa M, Shimizu T, Hara M, Onitsuka T. Source: European Journal of Surgical Oncology : the Journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology. 2003 October; 29(8): 654-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14511612&dopt=Abstract
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Prognostic significance of mutant p53 protein, P-glycoprotein and glutathione Stransferase-pi in patients with unresectable non-small cell lung cancer. Author(s): Miyatake K, Gemba K, Ueoka H, Nishii K, Kiura K, Tabata M, Shibayama T, Takigawa N, Kawaraya M, Tanimoto M. Source: Anticancer Res. 2003 May-June; 23(3C): 2829-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926120&dopt=Abstract
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Prognostic value of cytokeratin-positive cells in the bone marrow and lymph nodes of patients with resected nonsmall cell lung cancer: a multicenter prospective study. Author(s): Yasumoto K, Osaki T, Watanabe Y, Kato H, Yoshimura T. Source: The Annals of Thoracic Surgery. 2003 July; 76(1): 194-201; Discussion 202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842539&dopt=Abstract
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Prophylactic cranial irradiation for patients with locally advanced non-small-cell lung cancer. Author(s): Gore EM. Source: Oncology (Huntingt). 2003 June; 17(6): 775-9; Discussion 779-80, 784, 787 Passim. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846122&dopt=Abstract
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Proteomic patterns of tumour subsets in non-small-cell lung cancer. Author(s): Yanagisawa K, Shyr Y, Xu BJ, Massion PP, Larsen PH, White BC, Roberts JR, Edgerton M, Gonzalez A, Nadaf S, Moore JH, Caprioli RM, Carbone DP. Source: Lancet. 2003 August 9; 362(9382): 433-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12927430&dopt=Abstract
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Pulmonary embolism with cavity formation, spontaneous pneumothorax, and highoutput air leak in a patient with non-small-cell lung cancer. Author(s): Pavlakis G, Siafakas K, Gorgogiannis D, Sakorafas GH. Source: N Z Med J. 2003 July 11; 116(1177): 2P Following U500. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866506&dopt=Abstract
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Pulmonary paragonimiasis mimicking lung cancer on FDG-PET imaging. Author(s): Watanabe S, Nakamura Y, Kariatsumari K, Nagata T, Sakata R, Zinnouchi S, Date K. Source: Anticancer Res. 2003 July-August; 23(4): 3437-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926086&dopt=Abstract
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Quality of life after curative radiotherapy in Stage I non-small-cell lung cancer. Author(s): Langendijk JA, Aaronson NK, de Jong JM, ten Velde GP, Muller MJ, Slotman BJ, Wouters EF. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 July 15; 53(4): 847-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12095549&dopt=Abstract
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Quality of life after lung cancer surgery: a forgotten outcome measure. Author(s): Chen JC, Johnstone SA. Source: Chest. 2002 July; 122(1): 4-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12114328&dopt=Abstract
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Quality of life following lung cancer resection: video-assisted thoracic surgery vs thoracotomy. Author(s): Li WW, Lee TW, Lam SS, Ng CS, Sihoe AD, Wan IY, Yim AP. Source: Chest. 2002 August; 122(2): 584-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12171836&dopt=Abstract
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Quality of life following lung cancer surgery. Author(s): Myrdal G, Valtysdottir S, Lambe M, Stahle E. Source: Thorax. 2003 March; 58(3): 194-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612291&dopt=Abstract
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Quality of life of long-term survivors of non-small-cell lung cancer. Author(s): Sarna L, Padilla G, Holmes C, Tashkin D, Brecht ML, Evangelista L. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 July 1; 20(13): 2920-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089220&dopt=Abstract
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Quality trials and quality of life in non-small-cell lung cancer. Author(s): Harper P, Plunkett T, Khayat D. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3007-8. Epub 2003 July 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837809&dopt=Abstract
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Quantification of macrophage migration inhibitory factor mRNA expression in nonsmall cell lung cancer tissues and its clinical significance. Author(s): Tomiyasu M, Yoshino I, Suemitsu R, Okamoto T, Sugimachi K. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 December; 8(12): 3755-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473586&dopt=Abstract
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Quantitative O(6)-methylguanine DNA methyltransferase methylation analysis in curatively resected non-small cell lung cancer: associations with clinical outcome. Author(s): Brabender J, Usadel H, Metzger R, Schneider PM, Park J, Salonga D, TsaoWei DD, Groshen S, Lord RV, Takebe N, Schneider S, Holscher AH, Danenberg KD, Danenberg PV. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 January; 9(1): 223-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538473&dopt=Abstract
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RA175, which is the mouse ortholog of TSLC1, a tumor suppressor gene in human lung cancer, is a cell adhesion molecule. Author(s): Fujita E, Soyama A, Momoi T. Source: Experimental Cell Research. 2003 July 1; 287(1): 57-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799182&dopt=Abstract
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Racial differences pertaining to a belief about lung cancer surgery: results of a multicenter survey. Author(s): Margolis ML, Christie JD, Silvestri GA, Kaiser L, Santiago S, Hansen-Flaschen J. Source: Annals of Internal Medicine. 2003 October 7; 139(7): 558-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14530226&dopt=Abstract
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Radiation pneumonitis following treatment of non-small-cell lung cancer with continuous hyperfractionated accelerated radiotherapy (CHART). Author(s): Jenkins P, D'Amico K, Benstead K, Elyan S. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 June 1; 56(2): 360-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738310&dopt=Abstract
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Radiation therapy of changes secondary to lung cancer and pneumonectomy on bone and Tc-99m depreotide imaging. Author(s): Shih WJ, Kiefer V. Source: Clinical Nuclear Medicine. 2003 May; 28(5): 419-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702946&dopt=Abstract
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Radiologic screening for lung cancer. Author(s): Bastarrika G, Pueyo JC, Mulshine JL. Source: Expert Rev Anticancer Ther. 2002 August; 2(4): 385-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12647981&dopt=Abstract
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Radiotherapy for medically inoperable non-small cell lung cancer at clinical stage I and II. Author(s): Yamada K, Soejima T, Ota Y, Sasaki R, Yoden E, Kanaoka N, Maruta T, Sugimura K. Source: Tumori. 2003 January-February; 89(1): 75-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729366&dopt=Abstract
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RASSF1A gene inactivation in non-small cell lung cancer and its clinical implication. Author(s): Endoh H, Yatabe Y, Shimizu S, Tajima K, Kuwano H, Takahashi T, Mitsudomi T. Source: International Journal of Cancer. Journal International Du Cancer. 2003 August 10; 106(1): 45-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794755&dopt=Abstract
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Re: “Differential association of body mass index and fat distribution with three major histologic types of lung cancer: evidence from a cohort of older women”. Author(s): Kabir Z. Source: American Journal of Epidemiology. 2003 August 1; 158(3): 288; Author Reply 289. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882952&dopt=Abstract
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Re: “Dose specific meta-analysis and sensitivity analysis of the relation between alcohol consumption and lung cancer risk”. Author(s): Bandera EV, Potter JD. Source: American Journal of Epidemiology. 2003 March 15; 157(6): 569-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631550&dopt=Abstract
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Re: Beta-carotene and lung cancer: a lesson for future chemoprevention investigations? Author(s): Stram DO, Wu AH. Source: Journal of the National Cancer Institute. 2003 May 21; 95(10): E4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759404&dopt=Abstract
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Re: Double-blind, placebo-controlled, randomized phase III trial of darbepoetin alfa in lung cancer patients receiving chemotherapy. Author(s): VanAudenrode M. Source: Journal of the National Cancer Institute. 2003 May 21; 95(10): 761-2; Author Reply 762-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759400&dopt=Abstract
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Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic response to Bortezomib, a novel proteasome inhibitor, in human H460 non-small cell lung cancer cells. Author(s): Ling YH, Liebes L, Zou Y, Perez-Soler R. Source: The Journal of Biological Chemistry. 2003 September 5; 278(36): 33714-23. Epub 2003 June 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821677&dopt=Abstract
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Recurrent small cell lung cancer: update. Author(s): Glisson BS. Source: Seminars in Oncology. 2003 February; 30(1): 72-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635091&dopt=Abstract
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Reduced expression of the neuron restrictive silencer factor permits transcription of glycine receptor alpha1 subunit in small-cell lung cancer cells. Author(s): Gurrola-Diaz C, Lacroix J, Dihlmann S, Becker CM, von Knebel Doeberitz M. Source: Oncogene. 2003 August 28; 22(36): 5636-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944912&dopt=Abstract
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Reduction of cisplatin-induced anemia by the pineal indole 5-methoxytryptamine in metastatic lung cancer patients. Author(s): Lissoni P, Malugani F, Bukovec R, Bordin V, Perego M, Mengo S, Ardizzoia A, Tancini G. Source: Neuroendocrinol Lett. 2003 February-April; 24(1-2): 83-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743539&dopt=Abstract
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Remarks about usefulness of videothoracoscopic intrapericardial examination of pulmonary vessels to assess the resectability of clinical T4 lung cancer. Author(s): Wurtz AJ. Source: The Annals of Thoracic Surgery. 2003 July; 76(1): 342; Author Reply 342. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842588&dopt=Abstract
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Right lung cancer with right aortic arch. Author(s): Suzuki S, Miyamoto A, Aikawa H, Tabata T, Matsumura Y, Kondo T. Source: Jpn J Thorac Cardiovasc Surg. 2003 September; 51(9): 469-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14529170&dopt=Abstract
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Risk factors associated with lung cancer in Hong Kong. Author(s): Chan-Yeung M, Koo LC, Ho JC, Tsang KW, Chau WS, Chiu SW, Ip MS, Lam WK. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 131-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711113&dopt=Abstract
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Risk modification by CYP1A1 and GSTM1 polymorphisms in the association of environmental tobacco smoke and lung cancer: a case-control study in Japanese nonsmoking women. Author(s): Kiyohara C, Wakai K, Mikami H, Sido K, Ando M, Ohno Y. Source: International Journal of Cancer. Journal International Du Cancer. 2003 October 20; 107(1): 139-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925969&dopt=Abstract
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Role of Bcl-2 as a prognostic factor for survival in lung cancer: a systematic review of the literature with meta-analysis. Author(s): Martin B, Paesmans M, Berghmans T, Branle F, Ghisdal L, Mascaux C, Meert AP, Steels E, Vallot F, Verdebout JM, Lafitte JJ, Sculier JP. Source: British Journal of Cancer. 2003 July 7; 89(1): 55-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12838300&dopt=Abstract
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Role of skip metastasis to mediastinal lymph nodes in non-small cell lung cancer. Author(s): Prenzel KL, Monig SP, Sinning JM, Baldus SE, Gutschow CA, Grass G, Schneider PM, Holscher AH. Source: Journal of Surgical Oncology. 2003 April; 82(4): 256-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672010&dopt=Abstract
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Role of targeted therapy in non-small cell lung cancer: hype or hope? Author(s): Langer CJ. Source: Expert Rev Anticancer Ther. 2003 August; 3(4): 443-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934657&dopt=Abstract
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Routine use of approximately 60 Gy once-daily thoracic irradiation for patients with limited-stage small-cell lung cancer. Author(s): Miller KL, Marks LB, Sibley GS, Clough RW, Garst JL, Crawford J, Shafman TD. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 June 1; 56(2): 355-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738309&dopt=Abstract
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Scientists report progress against non-small cell lung cancer. Author(s): McCarthy M. Source: Lancet. 2003 June 14; 361(9374): 2055. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814725&dopt=Abstract
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Screening for lung cancer: a systematic review and meta-analysis of controlled trials. Author(s): Manser RL, Irving LB, Byrnes G, Abramson MJ, Stone CA, Campbell DA. Source: Thorax. 2003 September; 58(9): 784-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947138&dopt=Abstract
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Screening for lung cancer: an old idea revisited. Author(s): Sachs S. Source: Respir Care Clin N Am. 2003 March; 9(1): 27-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820711&dopt=Abstract
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Second-line chemotherapy for non-small cell lung cancer. Author(s): Shepherd FA. Source: Expert Rev Anticancer Ther. 2003 August; 3(4): 435-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934656&dopt=Abstract
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Sequence variations in the DNA repair gene XPD and risk of lung cancer in a Chinese population. Author(s): Liang G, Xing D, Miao X, Tan W, Yu C, Lu W, Lin D. Source: International Journal of Cancer. Journal International Du Cancer. 2003 July 10; 105(5): 669-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740916&dopt=Abstract
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Sequential chemoradiotherapy versus radiotherapy in the management of locally advanced non-small-cell lung cancer. Author(s): Sharma S, Sharma R, Bhowmik KT. Source: Adv Ther. 2003 January-February; 20(1): 14-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772814&dopt=Abstract
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Serial-measured versus estimated creatinine clearance in patients with non-small cell lung cancer receiving cisplatin-based chemotherapy. Author(s): Chang GC, Yang TY, Shih CM, Lin LY, Lee HS, Chiang CD. Source: J Formos Med Assoc. 2003 April; 102(4): 257-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833190&dopt=Abstract
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Small-cell cancers, and an unusual reaction to chemotherapy. Case 2. Synchronous renal cell carcinoma and limited-stage small-cell lung cancer. Author(s): Massarweh S, Lewitton M, Popat U, Lynch GR. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2439-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805345&dopt=Abstract
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Smoking, DNA repair capacity and risk of nonsmall cell lung cancer. Author(s): Shen H, Spitz MR, Qiao Y, Guo Z, Wang LE, Bosken CH, Amos CI, Wei Q. Source: International Journal of Cancer. Journal International Du Cancer. 2003 October 20; 107(1): 84-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925960&dopt=Abstract
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Some unusual paraneoplastic syndromes. Case 4. Paraneoplastic nephrotic syndrome in a patient with lung cancer. Author(s): Ebert B, Shaffer K, Rennke H. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2624-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829687&dopt=Abstract
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Staging of non-small-cell lung cancer with integrated PET and CT. Author(s): Pravinkumar E. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1188-90; Author Reply 1188-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14503543&dopt=Abstract
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Staging of non-small-cell lung cancer with integrated PET and CT. Author(s): Miles KA. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1188-90; Author Reply 1188-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14503542&dopt=Abstract
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Staging of non-small-cell lung cancer with integrated PET and CT. Author(s): Comans EF. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1188-90; Author Reply 1188-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14503541&dopt=Abstract
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Staging of non-small-cell lung cancer with integrated PET and CT. Author(s): Schirrmeister H, Hetzel M, Buck A. Source: The New England Journal of Medicine. 2003 September 18; 349(12): 1188-90; Author Reply 1188-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13679538&dopt=Abstract
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Staging of non-small-cell lung cancer with integrated positron-emission tomography and computed tomography. Author(s): Lardinois D, Weder W, Hany TF, Kamel EM, Korom S, Seifert B, von Schulthess GK, Steinert HC. Source: The New England Journal of Medicine. 2003 June 19; 348(25): 2500-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12815135&dopt=Abstract
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Stereotactic single-dose radiotherapy of stage I non-small-cell lung cancer (NSCLC). Author(s): Hof H, Herfarth KK, Munter M, Hoess A, Motsch J, Wannenmacher M, Debus J J. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 June 1; 56(2): 335-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738306&dopt=Abstract
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Strategies in lung cancer detection. Achieving early identification in patients at high risk. Author(s): Bechtel JJ, Petty TL. Source: Postgraduate Medicine. 2003 August; 114(2): 20-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926174&dopt=Abstract
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Strong association between the GSTM1-null genotype and lung cancer in a Turkish population. Author(s): Pinarbasi H, Silig Y, Cetinkaya O, Seyfikli Z, Pinarbasi E. Source: Cancer Genetics and Cytogenetics. 2003 October 15; 146(2): 125-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14553946&dopt=Abstract
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Study of lung cancer in MMVF workers. Author(s): Boffetta P, Kjaerheim K, Hansen J, Cherrie J, Chang-Claude J, Olsen JH, Saracci R, Westerholm P, Andersen A. Source: International Journal of Occupational and Environmental Health : Official Journal of the International Commission on Occupational Health. 2003 April-June; 9(2): 169-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848246&dopt=Abstract
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Surgical considerations with lung cancer screening. Author(s): Warner EE, Mulshine JL. Source: Journal of Surgical Oncology. 2003 September; 84(1): 1-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949983&dopt=Abstract
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Surgical management of cerebral metastases from non-small cell lung cancer. Author(s): Koutras AK, Marangos M, Kourelis T, Partheni M, Dougenis D, Iconomou G, Vagenakis AG, Kalofonos HP. Source: Tumori. 2003 May-June; 89(3): 292-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908786&dopt=Abstract
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Surgical viewpoints for the definitive treatment of lung cancer. Author(s): Bilfinger TV. Source: Respir Care Clin N Am. 2003 June; 9(2): 141-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911287&dopt=Abstract
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Survival among Chinese women with lung cancer in Singapore: a comparison by stage, histology and smoking status. Author(s): Tan YK, Wee TC, Koh WP, Wang YT, Eng P, Tan WC, Seow A. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 237-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781422&dopt=Abstract
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Survival and prognostic factors of surgically resected T4 non-small cell lung cancer. Author(s): Osaki T, Sugio K, Hanagiri T, Takenoyama M, Yamashita T, Sugaya M, Yasuda M, Yasumoto K. Source: The Annals of Thoracic Surgery. 2003 June; 75(6): 1745-51; Discussion 1751. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12822610&dopt=Abstract
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Survivin gene expression in early-stage non-small cell lung cancer. Author(s): Falleni M, Pellegrini C, Marchetti A, Oprandi B, Buttitta F, Barassi F, Santambrogio L, Coggi G, Bosari S. Source: The Journal of Pathology. 2003 August; 200(5): 620-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898598&dopt=Abstract
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Synchronous solitary fibrous tumor of the pleura and lung cancer. Author(s): Watanabe S, Nakamura Y, Sakasegawa K, Kariatsumari K, Yotsumoto D, Sakata R, Gezima K. Source: Anticancer Res. 2003 May-June; 23(3C): 2881-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926128&dopt=Abstract
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Targeted therapy for lung cancer. Author(s): Kukunoor R, Shah J, Mekhail T. Source: Current Oncology Reports. 2003 July; 5(4): 326-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781076&dopt=Abstract
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Targeted therapy in combination with gemcitabine in non-small cell lung cancer. Author(s): Rosell R, Crino L, Danenberg K, Scagliotti G, Bepler G, Taron M, Alberola V, Provencio M, Camps C, De Marinis F, Sanchez JJ, Penas R. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 10): 19-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917817&dopt=Abstract
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Temozolomide in patients with advanced non-small cell lung cancer with and without brain metastases. a phase II study of the EORTC Lung Cancer Group (08965). Author(s): Dziadziuszko R, Ardizzoni A, Postmus PE, Smit EF, Price A, Debruyne C, Legrand C, Giaccone G; EORTC Lung Cancer Group. Source: European Journal of Cancer (Oxford, England : 1990). 2003 June; 39(9): 1271-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763216&dopt=Abstract
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The cost-effectiveness of low-dose CT screening for lung cancer: preliminary results of baseline screening. Author(s): Wisnivesky JP, Mushlin AI, Sicherman N, Henschke C. Source: Chest. 2003 August; 124(2): 614-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907551&dopt=Abstract
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The emerging role of pemetrexed (Alimta) and gemcitabine in non-small cell lung cancer. Author(s): Le Chevalier T. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 10): 37-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947960&dopt=Abstract
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The impact of cardiovascular comorbidity on the outcome of surgery for stage I and II non-small-cell lung cancer. Author(s): Ambrogi V, Pompeo E, Elia S, Pistolese GR, Mineo TC. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 May; 23(5): 811-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754038&dopt=Abstract
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The natural history of recurrence after bronchoplastic procedures for non-small cell lung cancer. Author(s): Hollaus PH, Wurnig PN, Pridun NS. Source: The Annals of Thoracic Surgery. 2003 August; 76(2): 363-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902065&dopt=Abstract
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The Patterns of Care Study and Regional Cancer Registry for non-small-cell lung cancer in Japan. Author(s): Sugiyama H, Teshima T, Ohno Y, Inoue T, Takahashi Y, Oshima A, Sumi M, Uno T, Ikeda H; Japanese PCS Working Subgroup for Lung Cancer. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 July 15; 56(4): 1005-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829136&dopt=Abstract
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The rationale and potential of combining novel biologic therapies with radiotherapy: focus on non-small cell lung cancer. Author(s): Herbst RS, O'Reilly MS. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 9): 113-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908142&dopt=Abstract
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The re-emergence of aerosol gene delivery: a viable approach to lung cancer therapy. Author(s): Densmore CL. Source: Current Cancer Drug Targets. 2003 August; 3(4): 275-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871058&dopt=Abstract
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The relationship of pain, uncertainty, and hope in Taiwanese lung cancer patients. Author(s): Hsu TH, Lu MS, Tsou TS, Lin CC. Source: Journal of Pain and Symptom Management. 2003 September; 26(3): 835-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12967732&dopt=Abstract
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The role of chemotherapy in the treatment of unresectable stage III and IV nonsmall cell lung cancer. Author(s): Socinski MA. Source: Respir Care Clin N Am. 2003 June; 9(2): 207-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911290&dopt=Abstract
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The role of HER-2/neu expression on the survival of patients with lung cancer: a systematic review of the literature. Author(s): Meert AP, Martin B, Paesmans M, Berghmans T, Mascaux C, Verdebout JM, Delmotte P, Lafitte JJ, Sculier JP. Source: British Journal of Cancer. 2003 September 15; 89(6): 959-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966408&dopt=Abstract
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The role of mediastinoscopy in the evaluation of thoracic disease and lung cancer. Author(s): Hsu HS, Wang LS, Hsieh CC, Wang CY, Wu YC, Huang BS, Hsu WH, Huang MH. Source: J Chin Med Assoc. 2003 April; 66(4): 231-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854875&dopt=Abstract
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The role of mismatch repair in small-cell lung cancer cells. Author(s): Hansen LT, Thykjaer T, Orntoft TF, Rasmussen LJ, Keller P, Spang-Thomsen M, Edmonston TB, Schmutte C, Fishel R, Petersen LN. Source: European Journal of Cancer (Oxford, England : 1990). 2003 July; 39(10): 1456-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826050&dopt=Abstract
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The role of radiotherapy and chemotherapy for curative management of medically inoperable and stage III nonsmall cell lung cancer, and radiotherapy for palliation of symptomatic disease. Author(s): Turrisi AT 3rd, Bogart J, Sherman C, Silvestri G. Source: Respir Care Clin N Am. 2003 June; 9(2): 163-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911288&dopt=Abstract
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The sequence of vessel interruption during lobectomy for non-small cell lung cancer: is it indeed important? Author(s): Refaely Y, Sadetzki S, Chetrit A, Simansky DA, Paley M, Modan B, Yellin A. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 June; 125(6): 1313-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830050&dopt=Abstract
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The use of surgery to treat lung cancer in elderly patients. Author(s): Jaklitsch MT, Mery CM, Audisio RA. Source: The Lancet Oncology. 2003 August; 4(8): 463-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901960&dopt=Abstract
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The XRCC1 codon 399 Gln allele is associated with adenine to guanine p53 mutations in non-small cell lung cancer. Author(s): Casse C, Hu YC, Ahrendt SA. Source: Mutation Research. 2003 July 25; 528(1-2): 19-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873719&dopt=Abstract
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Thyroid transcription factor-1 expression prevalence and its clinical implications in non-small cell lung cancer: a high-throughput tissue microarray and immunohistochemistry study. Author(s): Tan D, Li Q, Deeb G, Ramnath N, Slocum HK, Brooks J, Cheney R, Wiseman S, Anderson T, Loewen G. Source: Human Pathology. 2003 June; 34(6): 597-604. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12827614&dopt=Abstract
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Transoesophageal echocardiography and lung cancer staging. Author(s): Maskill JM, Rother A, Seevanayagam S. Source: Thorax. 2003 August; 58(8): 735. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886001&dopt=Abstract
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Treatment of relapsed small-cell lung cancer--a focus on the evolving role of topotecan. Author(s): Rocha Lima CM, Chiappori A. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 229-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781421&dopt=Abstract
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Treatment options for brain metastases in patients with non-small-cell lung cancer. Author(s): Taimur S, Edelman MJ. Source: Current Oncology Reports. 2003 July; 5(4): 342-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781078&dopt=Abstract
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Treatment planning for lung cancer: traditional homogeneous point-dose prescription compared with heterogeneity-corrected dose-volume prescription. Author(s): Frank SJ, Forster KM, Stevens CW, Cox JD, Komaki R, Liao Z, Tucker S, Wang X, Steadham RE, Brooks C, Starkschall G. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 August 1; 56(5): 1308-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873675&dopt=Abstract
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Trends in histopathology of lung cancer in Alberta. Author(s): Hatcher J, Dover DC. Source: Canadian Journal of Public Health. Revue Canadienne De Sante Publique. 2003 July-August; 94(4): 292-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873089&dopt=Abstract
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Tumor implantation after pneumonectomy for lung cancer. Author(s): Raja V, Bessman D. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2998-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885823&dopt=Abstract
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Ubiquitination of tissue transglutaminase is modulated by interferon alpha in human lung cancer cells. Author(s): Esposito C, Marra M, Giuberti G, D'Alessandro AM, Porta R, Cozzolino A, Caraglia M, Abbruzzese A. Source: The Biochemical Journal. 2003 February 15; 370(Pt 1): 205-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401132&dopt=Abstract
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Uncommon syndromes and treatment manifestations of malignancy: Case 2. Metastatic non-small-cell lung cancer presenting with leukocytosis. Author(s): Ganti AK, Potti A, Mehdi S. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 January 1; 21(1): 168-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506187&dopt=Abstract
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Unsuspected residual disease at the resection margin after surgery for lung cancer: fate of patients after long-term follow-up. Author(s): Lequaglie C, Conti B, Brega Massone PP, Giudice G. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 February; 23(2): 229-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559347&dopt=Abstract
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Unusual presentations of lung cancer: Case 1. Diabetes insipidus as the initial manifestation of non-small-cell lung cancer. Author(s): Reddy P, Kalemkerian GP. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 1; 20(23): 4597-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454118&dopt=Abstract
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Unusual presentations of lung cancer: Case 2. Adrenal insufficiency as the initial manifestation of non-small-cell lung cancer. Author(s): Sirachainan E, Kalemkerian GP. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 1; 20(23): 4598-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454119&dopt=Abstract
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Unusual presentations of lung cancer: Case 3. Paraneoplastic digital necrosis in a patient with small-cell lung cancer. Author(s): Iamandi C, Dietemann A, Grosshans E, Pauli G, Quoix E. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 1; 20(23): 4600-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454120&dopt=Abstract
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Unusual presentations of lung cancer: Case 4. Palliative radiotherapy in eyelid nonHodgkin's lymphoma. Author(s): Galeazzi G, Di Russo A, Boffi R, De Conno F. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 1; 20(23): 4601-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454121&dopt=Abstract
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Unusual problems in breast cancer and a rare lung cancer case. Case 1. Clinical complete response of breast cancer metastases after trastuzumab-based immunotherapy. Author(s): Tonini G, Vincenzi B, Santini D, Avvisati G, La Cesa A, Baldi A. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2215-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775749&dopt=Abstract
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Unusual problems in breast cancer and a rare lung cancer case. Case 2. Aggressive fibromatosis of the chest wall arising near a breast prosthesis. Author(s): Khanfir K, Guinebretiere JM, Vanel D, Barreau-Pouhaer L, Bonvalot S, Le Cesne A. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2216-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775750&dopt=Abstract
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Unusual problems in breast cancer and a rare lung cancer case. Case 3. Simultaneous and synchronous bilateral inflammatory breast cancer. Author(s): Agrawal BL, Nath AR, Glynn TP Jr, Velazco D, Garnett RF Jr. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2218-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12784818&dopt=Abstract
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Unusual problems in breast cancer and a rare lung cancer case. Case 4. Primary lymphoepithelioma-like carcinoma of the lung. Author(s): Irie HY, Jaklitsch MT, Shaffer K, Weinstein M, Salgia R. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2220-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775751&dopt=Abstract
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Update on gemcitabine/carboplatin in patients with advanced non-small cell lung cancer. Author(s): Harper P. Source: Seminars in Oncology. 2003 August; 30(4 Suppl 10): 2-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917815&dopt=Abstract
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Update on the systemic treatment of lung cancer. Author(s): Giaccone G, Smit EF. Source: Cancer Chemother Biol Response Modif. 2002; 20: 697-716. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703231&dopt=Abstract
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Up-regulation of ALG-2 in hepatomas and lung cancer tissue. Author(s): la Cour JM, Mollerup J, Winding P, Tarabykina S, Sehested M, Berchtold MW. Source: American Journal of Pathology. 2003 July; 163(1): 81-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819013&dopt=Abstract
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Up-regulation of tumor interleukin-8 expression by infiltrating macrophages: its correlation with tumor angiogenesis and patient survival in non-small cell lung cancer. Author(s): Chen JJ, Yao PL, Yuan A, Hong TM, Shun CT, Kuo ML, Lee YC, Yang PC. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 February; 9(2): 729-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576442&dopt=Abstract
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Uptake rates of 18F-fluorodeoxyglucose and 11C-choline in lung cancer and pulmonary tuberculosis: a positron emission tomography study. Author(s): Hara T, Kosaka N, Suzuki T, Kudo K, Niino H. Source: Chest. 2003 September; 124(3): 893-901. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970014&dopt=Abstract
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Use of a dual-head coincidence camera and 18F-FDG for detection and nodal staging of non-small cell lung cancer: accuracy as determined by 2 independent observers. Author(s): Stevens H, Bakker PF, Schlosser NJ, van Rijk PP, de Klerk JM. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 March; 44(3): 336-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620997&dopt=Abstract
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Use of antisense oligonucleotides for therapy. Manipulation of apoptosis inhibitors for destruction of lung cancer cells. Author(s): Leech SH, Olie RA, Zangemeister-Wittke U. Source: Methods in Molecular Medicine. 2003; 75: 655-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407770&dopt=Abstract
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Use of ICD-9 coding as a proxy for stage of disease in lung cancer. Author(s): Thomas SK, Brooks SE, Mullins CD, Baquet CR, Merchant S. Source: Pharmacoepidemiology and Drug Safety. 2002 December; 11(8): 709-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512248&dopt=Abstract
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Use of nucleotide excision repair-deficient mice as a model for chemically induced lung cancer. Author(s): Cheo DL, Friedberg EC. Source: Methods in Molecular Medicine. 2003; 74: 481-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415716&dopt=Abstract
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Use of technetium-99m tin colloid for sentinel lymph node identification in nonsmall cell lung cancer. Author(s): Nomori H, Horio H, Naruke T, Orikasa H, Yamazaki K, Suemasu K. Source: The Journal of Thoracic and Cardiovascular Surgery. 2002 September; 124(3): 486-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12202864&dopt=Abstract
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Usefulness of bone markers for detection of bone metastases in lung cancer patients. Author(s): Alatas F, Alatas O, Metintas M, Colak O, Erginel S, Harmanci E. Source: Clinical Biochemistry. 2002 June; 35(4): 293-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12135691&dopt=Abstract
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Usefulness of low-dose spiral CT of the chest in regular follow-up of postoperative non-small cell lung cancer patients: Preliminary report. Author(s): Chiu CH, Chern MS, Wu MH, Hsu WH, Wu YC, Huang MH, Chang SC. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 June; 125(6): 1300-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830048&dopt=Abstract
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Using multiple imputation methods to estimate relative risks in small EPIC lung cancer subsets. Author(s): Altenburg HP, Agudo A, Berrino F, Boshuizen HC, Bueno-de-Mesquita HB, Janzon L, Le Marchand L, Linseisen J, Lukanova A, Rasmuson T, Vineis P, Riboli E, Miller A; EPIC Working Group on Lung Cancer. Source: Iarc Sci Publ. 2002; 156: 53-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12484123&dopt=Abstract
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Validation of the Charlson comorbidity index in patients with operated primary nonsmall cell lung cancer. Author(s): Birim O, Maat AP, Kappetein AP, van Meerbeeck JP, Damhuis RA, Bogers AJ. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 January; 23(1): 30-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12493500&dopt=Abstract
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Variations in lung cancer risk among smokers. Author(s): Bach PB, Kattan MW, Thornquist MD, Kris MG, Tate RC, Barnett MJ, Hsieh LJ, Begg CB. Source: Journal of the National Cancer Institute. 2003 March 19; 95(6): 470-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644540&dopt=Abstract
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Vascular endothelial growth factor expression in non-small cell lung cancer. Author(s): O'Byrne KJ, Goddard J, Giatromanolaki A, Koukourakis MI. Source: Methods in Molecular Medicine. 2003; 74: 357-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415708&dopt=Abstract
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Vegetables and fruits and lung cancer. Author(s): Miller AB; EPIC Working Group on Lung Cancer. Source: Iarc Sci Publ. 2002; 156: 85-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12484133&dopt=Abstract
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Video-assisted thoracic surgery (VATS) resection for lung cancer. Author(s): Swanson SJ, Batirel HF. Source: The Surgical Clinics of North America. 2002 June; 82(3): 541-59. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12371584&dopt=Abstract
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Vinorelbine and paclitaxel for locoregional advanced or metastatic non-small-cell lung cancer. Author(s): Perez JE, Machiavelli MR, Romero AO, Romero Acuna LA, Dominguez ME, Fasce H, Flores Acosta L, Marrone N, Romero Acuna JM, Langhi MJ, Amato S, Bologna F, Ortiz EH, Leone BA, Lacava JA, Vallejo CT. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2002 August; 25(4): 383-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12151970&dopt=Abstract
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Visceral pleura invasion and pleural lavage tumor cytology by lung cancer: a prospective appraisal. Author(s): Riquet M, Badoual C, Le Pimpec Barthes F, Lhote FM, Souilamas R, Hubsch JP, Danel C. Source: The Annals of Thoracic Surgery. 2003 February; 75(2): 353-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12607638&dopt=Abstract
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Wegener disease mimicking central lung cancer. Author(s): Cesario A, Meacci E, Mule A, Margaritora S. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2002 October; 22(4): 626. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12297184&dopt=Abstract
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What happens to patients undergoing lung cancer surgery? Outcomes and quality of life before and after surgery. Author(s): Handy JR Jr, Asaph JW, Skokan L, Reed CE, Koh S, Brooks G, Douville EC, Tsen AC, Ott GY, Silvestri GA. Source: Chest. 2002 July; 122(1): 21-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12114334&dopt=Abstract
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What margins are necessary for incorporating mediastinal nodal mobility into involved-field radiotherapy for lung cancer? Author(s): van Sornsen de Koste JR, Lagerwaard FJ, Nijssen-Visser MR, SchuchhardSchipper R, Joosten H, Senan S. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 August 1; 53(5): 1211-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12128122&dopt=Abstract
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Whole-body 18F-2-deoxyglucose positron emission tomography in primary staging small cell lung cancer. Author(s): Shen YY, Shiau YC, Wang JJ, Ho ST, Kao CH. Source: Anticancer Res. 2002 March-April; 22(2B): 1257-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12168935&dopt=Abstract
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Why are lung cancer rate trends so different in the United States and United kingdom? Author(s): Lee PN, Forey BA. Source: Inhalation Toxicology. 2003 August; 15(9): 909-49. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12872179&dopt=Abstract
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Will differential culturing of circulating human lung cancer cells aid in understanding metastasis? Author(s): Onuigbo WI. Source: Medical Hypotheses. 2002 June; 58(6): 552-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12323131&dopt=Abstract
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Will sewage workers with endotoxin related symptoms have the benefit of reduced lung cancer? Author(s): Lange JH, Mastrangelo G, Thomulka KW. Source: Occupational and Environmental Medicine. 2003 February; 60(2): 144-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554846&dopt=Abstract
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WNT7a induces E-cadherin in lung cancer cells. Author(s): Ohira T, Gemmill RM, Ferguson K, Kusy S, Roche J, Brambilla E, Zeng C, Baron A, Bemis L, Erickson P, Wilder E, Rustgi A, Kitajewski J, Gabrielson E, Bremnes R, Franklin W, Drabkin HA. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 September 2; 100(18): 10429-34. Epub 2003 August 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937339&dopt=Abstract
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Wortmannin inhibits growth of human non-small-cell lung cancer in vitro and in vivo. Author(s): Boehle AS, Kurdow R, Boenicke L, Schniewind B, Faendrich F, Dohrmann P, Kalthoff H. Source: Langenbeck's Archives of Surgery / Deutsche Gesellschaft Fur Chirurgie. 2002 October; 387(5-6): 234-9. Epub 2002 September 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410360&dopt=Abstract
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WW domain containing oxidoreductase gene expression is altered in non-small cell lung cancer. Author(s): Yendamuri S, Kuroki T, Trapasso F, Henry AC, Dumon KR, Huebner K, Williams NN, Kaiser LR, Croce CM. Source: Cancer Research. 2003 February 15; 63(4): 878-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12591741&dopt=Abstract
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XPA polymorphism associated with reduced lung cancer risk and a modulating effect on nucleotide excision repair capacity. Author(s): Wu X, Zhao H, Wei Q, Amos CI, Zhang K, Guo Z, Qiao Y, Hong WK, Spitz MR. Source: Carcinogenesis. 2003 March; 24(3): 505-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663511&dopt=Abstract
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ZD 1839 in patients with brain metastases from non-small-cell lung cancer (NSCLC): report of four cases. Author(s): Cappuzzo F, Calandri C, Bartolini S, Crino L. Source: British Journal of Cancer. 2003 July 21; 89(2): 246-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865910&dopt=Abstract
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ZD0473 treatment in lung cancer: an overview of the clinical trial results. Author(s): Treat J, Schiller J, Quoix E, Mauer A, Edelman M, Modiano M, Bonomi P, Ramlau R, Lemarie E. Source: European Journal of Cancer (Oxford, England : 1990). 2002 December; 38 Suppl 8: S13-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645908&dopt=Abstract
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ZD1839 (Iressa) in non-small cell lung cancer. Author(s): Herbst RS, Kies MS. Source: The Oncologist. 2002; 7 Suppl 4: 9-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12202783&dopt=Abstract
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ZD1839 (Iressa): for more than just non-small cell lung cancer. Author(s): Ranson M. Source: The Oncologist. 2002; 7 Suppl 4: 16-24. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12202784&dopt=Abstract
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ZD1839, a novel, oral epidermal growth factor receptor-tyrosine kinase inhibitor, as salvage treatment in patients with advanced non-small cell lung cancer. Experience from a single center participating in a compassionate use program. Author(s): Pallis AG, Mavroudis D, Androulakis N, Souglakos J, Kouroussis C, Bozionelou V, Vlachonikolis IG, Georgoulias V. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 301-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781429&dopt=Abstract
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Zoledronic acid versus placebo in the treatment of skeletal metastases in patients with lung cancer and other solid tumors: a phase III, double-blind, randomized trial-the Zoledronic Acid Lung Cancer and Other Solid Tumors Study Group. Author(s): Rosen LS, Gordon D, Tchekmedyian S, Yanagihara R, Hirsh V, Krzakowski M, Pawlicki M, de Souza P, Zheng M, Urbanowitz G, Reitsma D, Seaman JJ. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3150-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915606&dopt=Abstract
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CHAPTER 2. NUTRITION AND LUNG CANCER Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and lung cancer.
Finding Nutrition Studies on Lung Cancer The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “lung cancer” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on lung cancer: ·
A case-control study of lung cancer in Polish women. Author(s): Epidemiology Unit, Centre of Oncology, M. Sklodowska-Curie Memorial Institute, Cracow, Poland.
[email protected] Source: Rachtan, J Neoplasma. 2002; 49(2): 75-80 0028-2685
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A cohort study of dietary carotenoids and lung cancer risk in women (Canada). Author(s): Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
[email protected] Source: Rohan, T E Jain, M Howe, G R Miller, A B Cancer-Causes-Control. 2002 April; 13(3): 231-7 0957-5243
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A rapid and systematic review of the clinical effectiveness and cost-effectiveness of paclitaxel, docetaxel, gemcitabine and vinorelbine in non-small-cell lung cancer. Author(s): Southampton Health Technology Assessments Centre, Wessex Institute for Health Research and Development, University of Southampton, UK. Source: Clegg, A Scott, D A Sidhu, M Hewitson, P Waugh, N Health-Technol-Assess. 2001; 5(32): 1-195 1366-5278
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Aberrant promoter methylation in Chinese patients with non-small cell lung cancer: patterns in primary tumors and potential diagnostic application in bronchoalevolar lavage. Author(s): University Department of Medicine, Queen Mary Hospital, Hong Kong. Source: Chan, E C Lam, S Y Tsang, K W Lam, B Ho, J C Fu, K H Lam, W K Kwong, Y L Clin-Cancer-Res. 2002 December; 8(12): 3741-6 1078-0432
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Angiogenesis inhibitors in lung cancer. Author(s): Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 432, Houston 77030, USA.
[email protected] Source: Kim, Edward S Herbst, Roy S Curr-Oncol-Repage 2002 July; 4(4): 325-33 15233790
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Apoptosis of human highly metastatic lung cancer cell line 95-D induced by acutiaporberine, a novel bisalkaloid derived from Thalictrum acutifolium. Source: Chen, Q. Peng, W. Qi, S. Xu, A. Planta-med. Stuttgart : Georg Thieme Verlag,. June 2002. volume 68 (6) page 550-553. 0032-0943
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Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines in vitro and in vivo and produces synergistic growth inhibition in combination with other antitumor agents. Author(s): Lung Cancer Program of the University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver 80262, USA.
[email protected] Source: Chan, D C Gera, L Stewart, J M Helfrich, B Zhao, T L Feng, W Y Chan, K K Covey, J M Bunn, P A Jr Clin-Cancer-Res. 2002 May; 8(5): 1280-7 1078-0432
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Chemoprevention strategies for non-small cell lung cancer. Author(s): Netherlands Cancer Institute, Amsterdam, The Netherlands.
[email protected] Source: van Zandwijk, Nico Hirsch, Fred R Curr-Opin-Oncol. 2002 March; 14(2): 185-90 1040-8746
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Chemotherapy for small cell lung cancer. Author(s): Departments of Thoracic Oncology and Hematology/Oncology, Vanderbilt University, Nashville, TN 37232, USA. Source: Sandler, A B Semin-Oncol. 2003 February; 30(1): 9-25 0093-7754
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Chemotherapy of non-small cell lung cancer in elderly patients. Author(s): Division of Medical Oncology, S.G. Moscati Hospital, Avellino, Italy.
[email protected] Source: Gridelli, C Maione, P Colantuoni, G Rossi, A Curr-Med-Chem. 2002 August; 9(16): 1487-95 0929-8673
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Cigarette smoking and lung cancer: chemical mechanisms and approaches to prevention. Author(s): University of Minnesota Cancer Center, Minneapolis, MN 55455, USA.
[email protected] Source: Hecht, Stephen S Lancet-Oncol. 2002 August; 3(8): 461-9 1470-2045
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Comparison of unidimensional and bidimensional measurements in metastatic nonsmall cell lung cancer. Author(s): Department of Oncology, Clinica Universitaria de Navarra, Avenida de Pio XII, 36, 31008 Pamplona, Spain.
[email protected] Source: Cortes, J Rodriguez, J Diaz Gonzalez, J A Garzon, C Gurpide, A Arbea, L Gil Bazo, I Navarro, V Cambeiro, M Nicolas, A I Martin Algarra, S Garcia Foncillas, J Calvo, E Br-J-Cancer. 2002 July 15; 87(2): 158-60 0007-0920
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Concurrent administration of Docetaxel and Stealth liposomal doxorubicin with radiotherapy in non-small cell lung cancer : excellent tolerance using subcutaneous amifostine for cytoprotection. Author(s): Tumour and Angiogenesis Research Group, PO Box 12, Democritus University of Thrace, Alexandroupolis 68100, Greece.
[email protected] Source: Koukourakis, M I Romanidis, K Froudarakis, M Kyrgias, G Koukourakis, G V Retalis, G Bahlitzanakis, N Br-J-Cancer. 2002 August 12; 87(4): 385-92 0007-0920
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Cost-effectiveness of chemotherapy for nonsmall-cell lung cancer. Author(s): Cancer Care Ontario, Toronto, Canada. Source: Dranitsaris, G Cottrell, W Evans, W K Curr-Opin-Oncol. 2002 July; 14(4): 375-83 1040-8746
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Current role of irinotecan in the treatment of non-small-cell lung cancer. Author(s): Division of Medical Oncology, University of Colorado Health Sciences Center, Denver 80262, USA.
[email protected] Source: Kelly, K Oncology-(Huntingt). 2002 September; 16(9): 1153-62, 1165; discussion 1165-6 passim 0890-9091
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Dietary habits and lung cancer risk among Polish women. Author(s): Epidemiology Unit, Centre of Oncology, M. Sklodowska-Curie Memorial Institute, Cracow, Poland.
[email protected] Source: Rachtan, J Acta-Oncol. 2002; 41(4): 389-94 0284-186X
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Docetaxel followed by gemcitabine in the treatment of advanced non-small cell lung cancer: a phase I study. Author(s): Department of Medical Oncology, Pierantoni Hospital, Forli, Italy. Source: Frassineti, Giovanni Luca Ibrahim, Toni Zoli, Wainer Monti, Manuela Ricotti, Luca Nanni, Oriana Amadori, Dino Tumori. 2002 Mar-April; 88(2): 99-103 0300-8916
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Docetaxel in combination with platinums (cisplatin or carboplatin) in advanced and metastatic non-small cell lung cancer. Author(s): Lung and Thoracic Cancer Program, University of Pittsburgh Cancer Institute, PA. Source: Belani, Chandra P Semin-Oncol. 2002 June; 29(3 Suppl 12): 4-9 0093-7754
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Dose-escalation study of weekly irinotecan and daily carboplatin with concurrent thoracic radiotherapy for unresectable stage III non-small cell lung cancer. Author(s): First Department of Internal Medicine, Osaka City University Medical School, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
[email protected] Source: Yamada, M Kudoh, S Fukuda, H Nakagawa, K Yamamoto, N Nishimura, Y Negoro, S Takeda, K Tanaka, M Fukuoka, M Br-J-Cancer. 2002 July 29; 87(3): 258-63 0007-0920
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Early results of a randomized phase III trial of platinum-containing doublets versus a nonplatinum doublet in the treatment of advanced non-small cell lung cancer: European Organization for Research and Treatment of Cancer 08975. Author(s): Department of Medical Oncology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. Source: Giaccone, Giuseppe Semin-Oncol. 2002 June; 29(3 Suppl 9): 47-9 0093-7754
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Epidemiology, etiology, and prevention of lung cancer. Author(s): Department of Medicine, University of California San Francisco at Fresno, University Medical Center, Fresno, California, USA.
[email protected] Source: Bilello, Kathryn Smith Murin, Susan Matthay, Richard A Clin-Chest-Med. 2002 March; 23(1): 1-25 0272-5231
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Exisulind in combination with docetaxel inhibits growth and metastasis of human lung cancer and prolongs survival in athymic nude rats with orthotopic lung tumors. Author(s): University of Colorado Cancer Center, Department of Medicine, Preventive Medicine and Biostatistics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. Source: Chan, Daniel C Earle, Keith A Zhao, Tom L M Helfrich, Barbara Zeng, Chan Baron, Anna Whitehead, Clark M Piazza, Gary Pamukcu, Rifat Thompson, W Joseph Alila, Hector Nelson, Peter Bunn, Paul A Jr Clin-Cancer-Res. 2002 March; 8(3): 904-12 1078-0432
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Familial cancer aggregation and the risk of lung cancer. Author(s): Department of Epidemiology, Public Health School, University of Sao Paulo, Sao Paulo, Brazil.
[email protected] Source: Wunsch Filho, V Boffetta, P Colin, D Moncau, J E Sao-Paulo-Med-J. 2002 March 7; 120(2): 38-44 1516-3180
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GEM 231, a second-generation antisense agent complementary to protein kinase A RIalpha subunit, potentiates antitumor activity of irinotecan in human colon, pancreas, prostate and lung cancer xenografts. Author(s): Hybridon, Inc., Cambridge, MA 02139, USA.
[email protected] Source: Agrawal, S Kandimalla, E R Yu, D Ball, R Lombardi, G Lucas, T Dexter, D L Hollister, B A Chen, S F Int-J-Oncol. 2002 July; 21(1): 65-72 1019-6439
Nutrition 153
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Identification of a novel synthetic triterpenoid, methyl-2-cyano-3,12-dioxooleana-1,9dien-28-oate, that potently induces caspase-mediated apoptosis in human lung cancer cells. Author(s): Department of Thoracic/Head and Neck Medical Oncology, Box 432, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Source: Kim, K B Lotan, R Yue, P Sporn, M B Suh, N Gribble, G W Honda, T Wu, G S Hong, W K Sun, S Y Mol-Cancer-Ther. 2002 January; 1(3): 177-84 1535-7163
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Incorporation of pemetrexed (Alimta) into the treatment of non-small cell lung cancer (thoracic tumors). Author(s): Lung Cancer Program and Department of Medicine, University of Colorado Cancer Center and University of Colorado Health Sciences Center, Denver, CO 80262, USA. Source: Bunn, Paul A Jr Semin-Oncol. 2002 June; 29(3 Suppl 9): 17-22 0093-7754
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Insulin-like growth factor-I inhibits cell growth in the a549 non-small lung cancer cell line. Author(s): Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia. Source: Kodama, Y Baxter, R C Martin, J L Am-J-Respir-Cell-Mol-Biol. 2002 September; 27(3): 336-44 1044-1549
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Irinotecan in combination with radiation therapy for small-cell and non-small-cell lung cancer. Author(s): Center for Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-5671, USA. Source: Wu, H G Choy, H Oncology-(Huntingt). 2002 September; 16(9 Suppl 9): 13-8 0890-9091
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Irinotecan in the treatment of small cell lung cancer. Author(s): Department of Respiratory Disease, Otemae Hospital, 1-5-34 Otemae, Chuoku, Osaka, Osaka, 540-0008, Japan. Source: Masuda, N Fukuoka, M Expert-Rev-Anticancer-Ther. 2001 August; 1(2): 187-95 1473-7140
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Irinotecan plus cisplatin in small-cell lung cancer. Author(s): Division of Medical Oncology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-5536, USA.
[email protected] Source: Sandler, A Oncology-(Huntingt). 2002 September; 16(9 Suppl 9): 39-43 0890-9091
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Irinotecan therapy for small-cell lung cancer. Author(s): Vanderbilt University, Medical Center, Nashville, Tennessee 37232, USA. Source: Sandler, A Oncology-(Huntingt). 2002 April; 16(4): 419-25, 428, 433; discussion 433-4, 437-8 0890-9091
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Long-term follow-up of patients treated with paclitaxel/carboplatin-based chemotherapy for advanced non-small-cell lung cancer: sequential phase II trials of the Minnie Pearl Cancer Research Network. Author(s): Sarah Cannon Cancer Center and Tennessee Oncology, PLLC, Nashville, TN 37203, USA. Source: Hainsworth, John D Gray, James R Morrissey, Lisa H Kalman, Leonard A Hon, Jeremy K Greco, F Anthony J-Clin-Oncol. 2002 July 1; 20(13): 2937-42 0732-183X
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Lung cancer prevention with (-)-epigallocatechin gallate using monitoring by heterogeneous nuclear ribonucleoprotein B1. Author(s): Saitama Cancer Center, Ina, Kitaadachi-gun 362-0806, Japan. Source: Fujimoto, Nobukazu Sueoka, Naoko Sueoka, Eisaburo Okabe, Sachiko Suganuma, Masami Harada, Mine Fujiki, Hirota Int-J-Oncol. 2002 June; 20(6): 1233-9 1019-6439
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Mechanism of vinorelbine-induced radiosensitization of human small cell lung cancer cells. Author(s): Pharmacology Division, National Cancer Center Research Institute, Tokyo, Japan. Source: Fukuoka, Kazuya Arioka, Hitoshi Iwamoto, Yasuo Fukumoto, Hisao Kurokawa, Hirokazu Ishida, Tomoyuki Tomonari, Akira Suzuki, Toshihiro Usuda, Jitsuo Kanzawa, Fumihiko Kimura, Hiroshi Saijo, Nagahiro Nishio, Kazuto Cancer-ChemotherPharmacol. 2002 May; 49(5): 385-90 0344-5704
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New treatment approaches for lung cancer and impact on survival. Author(s): Oncology Department, Hospital Universitario, Madrid, Spain. Source: Cortes Funes, Hernan Semin-Oncol. 2002 June; 29(3 Suppl 8): 26-9 0093-7754
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Paclitaxel and carboplatin plus megestrol acetate in the treatment of advanced nonsmall cell lung cancer. Author(s): Department of Medicine, Faculty of Medicine, Chiang Mai University, Thailand. Source: Thongprasert, Sumitra Cheewakriangkrai, Rattiya Euathrongchit, Juntima Thaikla, Kanittha J-Med-Assoc-Thai. 2002 April; 85(4): 424-32 0125-2208
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Paclitaxel plus carboplatin versus gemcitabine plus paclitaxel in advanced non-smallcell lung cancer: a phase III randomized trial. Author(s): Second Medical Oncology Department, Hygeia Hospital, Athens, Greece.
[email protected] Source: Kosmidis, P Mylonakis, N Nicolaides, C Kalophonos, C Samantas, E Boukovinas, J Fountzilas, G Skarlos, D Economopoulos, T Tsavdaridis, D Papakostas, P Bacoyiannis, C Dimopoulos, M J-Clin-Oncol. 2002 September 1; 20(17): 3578-85 0732183X
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Pemetrexed as a single agent in the therapy of advanced lung cancer. Author(s): Department of Pulmonary Diseases, Vrije Universiteit, University Hospital Vrije Universiteit, Amsterdam, The Netherlands. Source: Postmus, Pieter E Bunn, Paul A Jr Semin-Oncol. 2002 April; 29(2 Suppl 5): 17-22 0093-7754
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Pemetrexed combination therapy in the treatment of non-small cell lung cancer. Author(s): Medical Oncology Service, Hospital Germans Trias i Pujol, Badalona, Barcelona, Spain. Source: Rosell, Rafael Crino, Lucio Semin-Oncol. 2002 April; 29(2 Suppl 5): 23-9 00937754
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Pemetrexed in the treatment of non-small cell lung cancer. Author(s): University of Toronto and the Princess Margaret Hospital, Toronto, ON, Canada. Source: Shepherd, F A Semin-Oncol. 2002 December; 29(6 Suppl 18): 43-8 0093-7754
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Perspectives and opportunities: Docetaxel in the current and future treatment of nonsmall cell lung cancer. Author(s): Department of Medicine, Medical University of South Carolina, Charleston 29425, USA. Source: Green, Mark R Semin-Oncol. 2002 June; 29(3 Suppl 12): 17-21 0093-7754
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Phase I/II study of gemcitabine plus vinorelbine in non-small cell lung cancer. Author(s): Medical Oncology Department, Hospital Central de Asturias, Oviedo, Spain.
[email protected] Source: Esteban, E Fra, J Corral, N Valle, M Carrasco, J Sala, M Puerta, J Estrada, E Palacio, I Vieitez, J M Buesa, J M Lacave, A J Invest-New-Drugs. 2002 February; 20(1): 73-82 0167-6997
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Phase II and pharmacologic study of weekly oral paclitaxel plus cyclosporine in patients with advanced non-small-cell lung cancer. Author(s): Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands. Source: Kruijtzer, C M Schellens, J H Mezger, J Scheulen, M E Keilholz, U Beijnen, J H Rosing, H Mathot, R A Marcus, S van Tinteren, H Baas, P J-Clin-Oncol. 2002 December 1; 20(23): 4508-16 0732-183X
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Phase II neoadjuvant trial of paclitaxel by 96-hour continuous infusion (CIVI) in combination with cisplatin followed by chest radiotherapy for patients with stage III non-small-cell lung cancer. Author(s): Medicine Branch, Division of Clinical Sciences, National Cancer Institute (NCI)/National Naval Medical Center, NNMC, Bethesda, Maryland, USA. Source: Breathnach, O S Kasturi, V Kaye, F Herscher, L Georgiadis, M S Edison, M Schuler, B S Pizzella, P Steinberg, S M O'Neil, K Johnson, Bruce E Am-J-Clin-Oncol. 2002 June; 25(3): 269-73 0277-3732
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Phase II study of docetaxel and cisplatin combination chemotherapy in metastatic or unresectable localized non-small-cell lung cancer. Author(s): Department of Internal Medicine, Korea University, College of Medicine, Seoul, Korea. Source: Kim, Y H Kim, J S Choi, Y H In, K H Park, H S Hong, D S Jeong, T J Lee, Y Y Nam, E Lee, S N Lee, K S Kim, H K Int-J-Clin-Oncol. 2002 April; 7(2): 114-9 1341-9625
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Phase II study of docetaxel and gemcitabine combination chemotherapy in nonsmall-cell lung cancer patients failing previous chemotherapy. Author(s): Chest Department, Taipei Veterans General Hospital, and School of Medicine, National Yang-Ming University, Taipei 112, Taiwan, ROC. Source: Chen, Y M Perng, R P Lin, W C Wu, H W Tsai, C M Whang Peng, J Am-J-ClinOncol. 2002 October; 25(5): 509-12 0277-3732
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Phase III randomized trial comparing three platinum-based doublets in advanced non-small-cell lung cancer. Author(s): Department of Clinical and Biological Sciences, University of Torino, Turin.
[email protected] Source: Scagliotti, G V De Marinis, F Rinaldi, M Crino, L Gridelli, C Ricci, S Matano, E Boni, C Marangolo, M Failla, G Altavilla, G Adamo, V Ceribelli, A Clerici, M Di Costanzo, F Frontini, L Tonato, M J-Clin-Oncol. 2002 November 1; 20(21): 4285-91 0732183X
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Platinum drugs in the treatment of non-small-cell lung cancer. Author(s): AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK.
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Source: Cosaert, J Quoix, E Br-J-Cancer. 2002 October 7; 87(8): 825-33 0007-0920 ·
Randomised phase III trial of irinotecan combined with cisplatin for advanced nonsmall-cell lung cancer. Author(s): Department of Clinical Oncology, Osaka City General Hospital, Osaka, Japan.
[email protected] Source: Negoro, S Masuda, N Takada, Y Sugiura, T Kudoh, S Katakami, N Ariyoshi, Y Ohashi, Y Niitani, H Fukuoka, M Br-J-Cancer. 2003 February 10; 88(3): 335-41 0007-0920
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): University of Chicago Medical Center and Cancer and Leukemia Group B, Chicago, IL, USA.
[email protected] Source: Vokes, E E Herndon, J E 2nd Crawford, J Leopold, K A Perry, M C Miller, A A Green, M R J-Clin-Oncol. 2002 October 15; 20(20): 4191-8 0732-183X
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Real-time polymerase chain reaction monitoring of epithelial cell adhesion moleculeinduced T-cell stimulation in patients with lung cancer and healthy individuals using LightCycler technology. Author(s): Division of Oncology, Department of Internal Medicine, University Hospital Zurich, Ramistrasse 100, CH-8091 Zurich, Switzerland.
[email protected] Source: TroJanuary, A Urosevic, M Dummer, R Nestle, F O Stahel, R A J-Immunother. 2002 May-June; 25(3): 264-8 1524-9557
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Recombinant human interleukin-3 administered concomitantly with chemotherapy in patients with relapsed small cell lung cancer. Author(s): Department of Pulmonology, University Hospital, Free University of Amsterdam, The Netherlands. Source: Biesma, B van Kralingen, K W van Leen, R W Koster, M C Postmus, P E J-ExpTher-Oncol. 2002 Jan-February; 2(1): 47-52 1359-4117
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Risk factors for lung cancer among Canadian women who have never smoked. Author(s): Centre for Chronic Disease Prevention and Control, Population and Public Health Brance, Health Canada, Ottawa, Ont. Source: Hu, J Mao, Y Dryer, D White, K Cancer-Detect-Prevolume 2002; 26(2): 129-38 0361-090X
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Salvage chemotherapy with the gemcitabine/docetaxel combination in non-small cell lung cancer: an overview of recent phase II studies. Author(s): Department of Medicine, Medical Oncology Unit, Helena-Venizelou Hospital, Athens, Greece.
[email protected] Source: Kosmas, C Tsavaris, N Kalofonos, H P Med-Sci-Monit. 2002 June; 8(6): PI58-63 1234-1010
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Second-line chemotherapy with irinotecan and vinorelbine in stage IIIB and IV nonsmall-cell lung cancer: a phase II study. Author(s): Department of Oncology, Clinica Universitaria de Navarra, University of Navarra, Spain. Source: Gonzalez Cao, M Aramendia, J M Salgado, E Aristu, J Martinez Monje, R Algarra, S M Ordonez, J M Brugarolas, A Am-J-Clin-Oncol. 2002 October; 25(5): 480-4 0277-3732
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Selective oral epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 is generally well-tolerated and has activity in non-small-cell lung cancer and other solid tumors: results of a phase I trial. Author(s): Department of Thoracic/Head and Neck Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA. Source: Herbst, R S Maddox, A M Rothenberg, M L Small, E J Rubin, E H Baselga, J Rojo, F Hong, W K Swaisland, H Averbuch, S D Ochs, J LoRusso, P M J-Clin-Oncol. 2002 September 15; 20(18): 3815-25 0732-183X
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Significant growth inhibition of human lung cancer cells both in vitro and in vivo by the combined use of a selective cyclooxygenase 2 inhibitor, JTE-522, and conventional anticancer agents. Author(s): Department of Internal Medicine, Aichi Cancer Center Hospital, Nagoya 4648681, Japan.
[email protected] Source: Hida, T Kozaki, K Ito, H Miyaishi, O Tatematsu, Y Suzuki, T Matsuo, K Sugiura, T Ogawa, M Takahashi, T Takahashi, T Clin-Cancer-Res. 2002 July; 8(7): 2443-7 10780432
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Slow metabolism and long half life of methadone in a patient with lung cancer and cirrhosis. Author(s): Pharmacie, Hopital Paul-Guiraud, 54, avenue de la Republique, 94806 Villejuif Cedex.
[email protected] Source: Beauverie, P Furlan, V Edel, Y A Ann-Med-Interne-(Paris). 2001 November; 152 Suppl 7: 50-2 0003-410X
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The case for the introduction of new chemotherapy agents in the treatment of advanced non small cell lung cancer in the wake of the findings of The National Institute of Clinical Excellence (NICE). Author(s): Lung Unit, The Royal Marsden Hospital, Sutton, Surrey, UK. Source: Waters, J S O'Brien, M E Br-J-Cancer. 2002 August 27; 87(5): 481-90 0007-0920
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The role of carotenoids on the risk of lung cancer. Author(s): Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. Source: Epstein, K R Semin-Oncol. 2003 February; 30(1): 86-93 0093-7754
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Tumor lysis syndrome in extensive-stage small-cell lung cancer. Author(s): Department of Radiation Oncology, MS 200, Hahnemann University Hospital, Broad and Vine Street, Philadelphia, PA 19102, USA. Source: Beriwal, S Singh, S Garcia Young, J A Am-J-Clin-Oncol. 2002 October; 25(5): 4745 0277-3732
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Vinorelbine and paclitaxel for locoregional advanced or metastatic non-small-cell lung cancer. Author(s): Grupo Oncologico Cooperativo del Sur (G.O.C.S.), Republica Argentina. Source: Perez, Juan E Machiavelli, Mario R Romero, Alberto O Romero Acuna, Luis A Dominguez, Maria E Fasce, Hebe Flores Acosta, Luis Marrone, Nora Romero Acuna, Juan M Langhi, Mario J Amato, Sonia Bologna, Fabrina Ortiz, Eduardo H Leone, Bernardo A Lacava, Juan A Vallejo, Carlos T Am-J-Clin-Oncol. 2002 August; 25(4): 383-7 0277-3732
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Vinorelbine in the treatment of non-small cell lung cancer. Author(s): Divisione di Oncologia Medica, Azienda Ospedaliera S.G.Moscati, Avellino, Italy.
[email protected] Source: Gridelli, C De Vivo, R Curr-Med-Chem. 2002 April; 9(8): 879-91 0929-8673
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ZD1839 (Iressa) in non-small cell lung cancer. Author(s): Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Herbst, R S Kies, M S Oncologist. 2002; 7 Suppl 4: 9-15 1083-7159
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ZD1839 (Iressa): for more than just non-small cell lung cancer. Author(s): Department of Medical Oncology, Christie Hospital NHS Trust, Manchester, United Kingdom.
[email protected] Source: Ranson, M Oncologist. 2002; 7 Suppl 4: 16-24 1083-7159
The following information is typical of that found when using the “Full IBIDS Database” to search for “lung cancer” (or a synonym): ·
A case-control study of lung cancer in Polish women. Author(s): Epidemiology Unit, Centre of Oncology, M. Sklodowska-Curie Memorial Institute, Cracow, Poland.
[email protected] Source: Rachtan, J Neoplasma. 2002; 49(2): 75-80 0028-2685
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A cohort study of dietary carotenoids and lung cancer risk in women (Canada). Author(s): Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
[email protected] Source: Rohan, T E Jain, M Howe, G R Miller, A B Cancer-Causes-Control. 2002 April; 13(3): 231-7 0957-5243
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A rapid and systematic review of the clinical effectiveness and cost-effectiveness of paclitaxel, docetaxel, gemcitabine and vinorelbine in non-small-cell lung cancer. Author(s): Southampton Health Technology Assessments Centre, Wessex Institute for Health Research and Development, University of Southampton, UK. Source: Clegg, A Scott, D A Sidhu, M Hewitson, P Waugh, N Health-Technol-Assess. 2001; 5(32): 1-195 1366-5278
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Aberrant promoter methylation in Chinese patients with non-small cell lung cancer: patterns in primary tumors and potential diagnostic application in bronchoalevolar lavage. Author(s): University Department of Medicine, Queen Mary Hospital, Hong Kong. Source: Chan, E C Lam, S Y Tsang, K W Lam, B Ho, J C Fu, K H Lam, W K Kwong, Y L Clin-Cancer-Res. 2002 December; 8(12): 3741-6 1078-0432
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Angiogenesis inhibitors in lung cancer. Author(s): Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 432, Houston 77030, USA.
[email protected] Source: Kim, Edward S Herbst, Roy S Curr-Oncol-Repage 2002 July; 4(4): 325-33 15233790
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Apoptosis of human highly metastatic lung cancer cell line 95-D induced by acutiaporberine, a novel bisalkaloid derived from Thalictrum acutifolium. Source: Chen, Q. Peng, W. Qi, S. Xu, A. Planta-med. Stuttgart : Georg Thieme Verlag,. June 2002. volume 68 (6) page 550-553. 0032-0943
Nutrition 159
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Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines in vitro and in vivo and produces synergistic growth inhibition in combination with other antitumor agents. Author(s): Lung Cancer Program of the University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver 80262, USA.
[email protected] Source: Chan, D C Gera, L Stewart, J M Helfrich, B Zhao, T L Feng, W Y Chan, K K Covey, J M Bunn, P A Jr Clin-Cancer-Res. 2002 May; 8(5): 1280-7 1078-0432
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Chemoprevention strategies for non-small cell lung cancer. Author(s): Netherlands Cancer Institute, Amsterdam, The Netherlands.
[email protected] Source: van Zandwijk, Nico Hirsch, Fred R Curr-Opin-Oncol. 2002 March; 14(2): 185-90 1040-8746
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Chemotherapy for small cell lung cancer. Author(s): Departments of Thoracic Oncology and Hematology/Oncology, Vanderbilt University, Nashville, TN 37232, USA. Source: Sandler, A B Semin-Oncol. 2003 February; 30(1): 9-25 0093-7754
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Chemotherapy of non-small cell lung cancer in elderly patients. Author(s): Division of Medical Oncology, S.G. Moscati Hospital, Avellino, Italy.
[email protected] Source: Gridelli, C Maione, P Colantuoni, G Rossi, A Curr-Med-Chem. 2002 August; 9(16): 1487-95 0929-8673
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Cigarette smoking and lung cancer: chemical mechanisms and approaches to prevention. Author(s): University of Minnesota Cancer Center, Minneapolis, MN 55455, USA.
[email protected] Source: Hecht, Stephen S Lancet-Oncol. 2002 August; 3(8): 461-9 1470-2045
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Comparison of unidimensional and bidimensional measurements in metastatic nonsmall cell lung cancer. Author(s): Department of Oncology, Clinica Universitaria de Navarra, Avenida de Pio XII, 36, 31008 Pamplona, Spain.
[email protected] Source: Cortes, J Rodriguez, J Diaz Gonzalez, J A Garzon, C Gurpide, A Arbea, L Gil Bazo, I Navarro, V Cambeiro, M Nicolas, A I Martin Algarra, S Garcia Foncillas, J Calvo, E Br-J-Cancer. 2002 July 15; 87(2): 158-60 0007-0920
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Concurrent administration of Docetaxel and Stealth liposomal doxorubicin with radiotherapy in non-small cell lung cancer : excellent tolerance using subcutaneous amifostine for cytoprotection. Author(s): Tumour and Angiogenesis Research Group, PO Box 12, Democritus University of Thrace, Alexandroupolis 68100, Greece.
[email protected] Source: Koukourakis, M I Romanidis, K Froudarakis, M Kyrgias, G Koukourakis, G V Retalis, G Bahlitzanakis, N Br-J-Cancer. 2002 August 12; 87(4): 385-92 0007-0920
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Cost-effectiveness of chemotherapy for nonsmall-cell lung cancer. Author(s): Cancer Care Ontario, Toronto, Canada. Source: Dranitsaris, G Cottrell, W Evans, W K Curr-Opin-Oncol. 2002 July; 14(4): 375-83 1040-8746
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Current role of irinotecan in the treatment of non-small-cell lung cancer. Author(s): Division of Medical Oncology, University of Colorado Health Sciences Center, Denver 80262, USA.
[email protected] 160 Lung Cancer
Source: Kelly, K Oncology-(Huntingt). 2002 September; 16(9): 1153-62, 1165; discussion 1165-6 passim 0890-9091 ·
Dietary habits and lung cancer risk among Polish women. Author(s): Epidemiology Unit, Centre of Oncology, M. Sklodowska-Curie Memorial Institute, Cracow, Poland.
[email protected] Source: Rachtan, J Acta-Oncol. 2002; 41(4): 389-94 0284-186X
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Docetaxel followed by gemcitabine in the treatment of advanced non-small cell lung cancer: a phase I study. Author(s): Department of Medical Oncology, Pierantoni Hospital, Forli, Italy. Source: Frassineti, Giovanni Luca Ibrahim, Toni Zoli, Wainer Monti, Manuela Ricotti, Luca Nanni, Oriana Amadori, Dino Tumori. 2002 Mar-April; 88(2): 99-103 0300-8916
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Docetaxel in combination with platinums (cisplatin or carboplatin) in advanced and metastatic non-small cell lung cancer. Author(s): Lung and Thoracic Cancer Program, University of Pittsburgh Cancer Institute, PA. Source: Belani, Chandra P Semin-Oncol. 2002 June; 29(3 Suppl 12): 4-9 0093-7754
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Dose-escalation study of weekly irinotecan and daily carboplatin with concurrent thoracic radiotherapy for unresectable stage III non-small cell lung cancer. Author(s): First Department of Internal Medicine, Osaka City University Medical School, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
[email protected] Source: Yamada, M Kudoh, S Fukuda, H Nakagawa, K Yamamoto, N Nishimura, Y Negoro, S Takeda, K Tanaka, M Fukuoka, M Br-J-Cancer. 2002 July 29; 87(3): 258-63 0007-0920
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Early results of a randomized phase III trial of platinum-containing doublets versus a nonplatinum doublet in the treatment of advanced non-small cell lung cancer: European Organization for Research and Treatment of Cancer 08975. Author(s): Department of Medical Oncology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. Source: Giaccone, Giuseppe Semin-Oncol. 2002 June; 29(3 Suppl 9): 47-9 0093-7754
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Epidemiology, etiology, and prevention of lung cancer. Author(s): Department of Medicine, University of California San Francisco at Fresno, University Medical Center, Fresno, California, USA.
[email protected] Source: Bilello, Kathryn Smith Murin, Susan Matthay, Richard A Clin-Chest-Med. 2002 March; 23(1): 1-25 0272-5231
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Exisulind in combination with docetaxel inhibits growth and metastasis of human lung cancer and prolongs survival in athymic nude rats with orthotopic lung tumors. Author(s): University of Colorado Cancer Center, Department of Medicine, Preventive Medicine and Biostatistics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. Source: Chan, Daniel C Earle, Keith A Zhao, Tom L M Helfrich, Barbara Zeng, Chan Baron, Anna Whitehead, Clark M Piazza, Gary Pamukcu, Rifat Thompson, W Joseph Alila, Hector Nelson, Peter Bunn, Paul A Jr Clin-Cancer-Res. 2002 March; 8(3): 904-12 1078-0432
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Familial cancer aggregation and the risk of lung cancer. Author(s): Department of Epidemiology, Public Health School, University of Sao Paulo, Sao Paulo, Brazil.
[email protected] Nutrition 161
Source: Wunsch Filho, V Boffetta, P Colin, D Moncau, J E Sao-Paulo-Med-J. 2002 March 7; 120(2): 38-44 1516-3180 ·
GEM 231, a second-generation antisense agent complementary to protein kinase A RIalpha subunit, potentiates antitumor activity of irinotecan in human colon, pancreas, prostate and lung cancer xenografts. Author(s): Hybridon, Inc., Cambridge, MA 02139, USA.
[email protected] Source: Agrawal, S Kandimalla, E R Yu, D Ball, R Lombardi, G Lucas, T Dexter, D L Hollister, B A Chen, S F Int-J-Oncol. 2002 July; 21(1): 65-72 1019-6439
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Identification of a novel synthetic triterpenoid, methyl-2-cyano-3,12-dioxooleana-1,9dien-28-oate, that potently induces caspase-mediated apoptosis in human lung cancer cells. Author(s): Department of Thoracic/Head and Neck Medical Oncology, Box 432, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Source: Kim, K B Lotan, R Yue, P Sporn, M B Suh, N Gribble, G W Honda, T Wu, G S Hong, W K Sun, S Y Mol-Cancer-Ther. 2002 January; 1(3): 177-84 1535-7163
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Incorporation of pemetrexed (Alimta) into the treatment of non-small cell lung cancer (thoracic tumors). Author(s): Lung Cancer Program and Department of Medicine, University of Colorado Cancer Center and University of Colorado Health Sciences Center, Denver, CO 80262, USA. Source: Bunn, Paul A Jr Semin-Oncol. 2002 June; 29(3 Suppl 9): 17-22 0093-7754
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Insulin-like growth factor-I inhibits cell growth in the a549 non-small lung cancer cell line. Author(s): Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia. Source: Kodama, Y Baxter, R C Martin, J L Am-J-Respir-Cell-Mol-Biol. 2002 September; 27(3): 336-44 1044-1549
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Irinotecan in combination with radiation therapy for small-cell and non-small-cell lung cancer. Author(s): Center for Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-5671, USA. Source: Wu, H G Choy, H Oncology-(Huntingt). 2002 September; 16(9 Suppl 9): 13-8 0890-9091
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Irinotecan in the treatment of small cell lung cancer. Author(s): Department of Respiratory Disease, Otemae Hospital, 1-5-34 Otemae, Chuoku, Osaka, Osaka, 540-0008, Japan. Source: Masuda, N Fukuoka, M Expert-Rev-Anticancer-Ther. 2001 August; 1(2): 187-95 1473-7140
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Irinotecan plus cisplatin in small-cell lung cancer. Author(s): Division of Medical Oncology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-5536, USA.
[email protected] Source: Sandler, A Oncology-(Huntingt). 2002 September; 16(9 Suppl 9): 39-43 0890-9091
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Irinotecan therapy for small-cell lung cancer. Author(s): Vanderbilt University, Medical Center, Nashville, Tennessee 37232, USA. Source: Sandler, A Oncology-(Huntingt). 2002 April; 16(4): 419-25, 428, 433; discussion 433-4, 437-8 0890-9091
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Long-term follow-up of patients treated with paclitaxel/carboplatin-based chemotherapy for advanced non-small-cell lung cancer: sequential phase II trials of the Minnie Pearl Cancer Research Network. Author(s): Sarah Cannon Cancer Center and Tennessee Oncology, PLLC, Nashville, TN 37203, USA. Source: Hainsworth, John D Gray, James R Morrissey, Lisa H Kalman, Leonard A Hon, Jeremy K Greco, F Anthony J-Clin-Oncol. 2002 July 1; 20(13): 2937-42 0732-183X
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Lung cancer prevention with (-)-epigallocatechin gallate using monitoring by heterogeneous nuclear ribonucleoprotein B1. Author(s): Saitama Cancer Center, Ina, Kitaadachi-gun 362-0806, Japan. Source: Fujimoto, Nobukazu Sueoka, Naoko Sueoka, Eisaburo Okabe, Sachiko Suganuma, Masami Harada, Mine Fujiki, Hirota Int-J-Oncol. 2002 June; 20(6): 1233-9 1019-6439
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Mechanism of vinorelbine-induced radiosensitization of human small cell lung cancer cells. Author(s): Pharmacology Division, National Cancer Center Research Institute, Tokyo, Japan. Source: Fukuoka, Kazuya Arioka, Hitoshi Iwamoto, Yasuo Fukumoto, Hisao Kurokawa, Hirokazu Ishida, Tomoyuki Tomonari, Akira Suzuki, Toshihiro Usuda, Jitsuo Kanzawa, Fumihiko Kimura, Hiroshi Saijo, Nagahiro Nishio, Kazuto Cancer-ChemotherPharmacol. 2002 May; 49(5): 385-90 0344-5704
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New treatment approaches for lung cancer and impact on survival. Author(s): Oncology Department, Hospital Universitario, Madrid, Spain. Source: Cortes Funes, Hernan Semin-Oncol. 2002 June; 29(3 Suppl 8): 26-9 0093-7754
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Paclitaxel and carboplatin plus megestrol acetate in the treatment of advanced nonsmall cell lung cancer. Author(s): Department of Medicine, Faculty of Medicine, Chiang Mai University, Thailand. Source: Thongprasert, Sumitra Cheewakriangkrai, Rattiya Euathrongchit, Juntima Thaikla, Kanittha J-Med-Assoc-Thai. 2002 April; 85(4): 424-32 0125-2208
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Paclitaxel plus carboplatin versus gemcitabine plus paclitaxel in advanced non-smallcell lung cancer: a phase III randomized trial. Author(s): Second Medical Oncology Department, Hygeia Hospital, Athens, Greece.
[email protected] Source: Kosmidis, P Mylonakis, N Nicolaides, C Kalophonos, C Samantas, E Boukovinas, J Fountzilas, G Skarlos, D Economopoulos, T Tsavdaridis, D Papakostas, P Bacoyiannis, C Dimopoulos, M J-Clin-Oncol. 2002 September 1; 20(17): 3578-85 0732183X
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Pemetrexed as a single agent in the therapy of advanced lung cancer. Author(s): Department of Pulmonary Diseases, Vrije Universiteit, University Hospital Vrije Universiteit, Amsterdam, The Netherlands. Source: Postmus, Pieter E Bunn, Paul A Jr Semin-Oncol. 2002 April; 29(2 Suppl 5): 17-22 0093-7754
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Pemetrexed combination therapy in the treatment of non-small cell lung cancer. Author(s): Medical Oncology Service, Hospital Germans Trias i Pujol, Badalona, Barcelona, Spain. Source: Rosell, Rafael Crino, Lucio Semin-Oncol. 2002 April; 29(2 Suppl 5): 23-9 00937754
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Pemetrexed in the treatment of non-small cell lung cancer. Author(s): University of Toronto and the Princess Margaret Hospital, Toronto, ON, Canada. Source: Shepherd, F A Semin-Oncol. 2002 December; 29(6 Suppl 18): 43-8 0093-7754
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Perspectives and opportunities: Docetaxel in the current and future treatment of nonsmall cell lung cancer. Author(s): Department of Medicine, Medical University of South Carolina, Charleston 29425, USA. Source: Green, Mark R Semin-Oncol. 2002 June; 29(3 Suppl 12): 17-21 0093-7754
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Phase I/II study of gemcitabine plus vinorelbine in non-small cell lung cancer. Author(s): Medical Oncology Department, Hospital Central de Asturias, Oviedo, Spain.
[email protected] Source: Esteban, E Fra, J Corral, N Valle, M Carrasco, J Sala, M Puerta, J Estrada, E Palacio, I Vieitez, J M Buesa, J M Lacave, A J Invest-New-Drugs. 2002 February; 20(1): 73-82 0167-6997
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Phase II and pharmacologic study of weekly oral paclitaxel plus cyclosporine in patients with advanced non-small-cell lung cancer. Author(s): Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands. Source: Kruijtzer, C M Schellens, J H Mezger, J Scheulen, M E Keilholz, U Beijnen, J H Rosing, H Mathot, R A Marcus, S van Tinteren, H Baas, P J-Clin-Oncol. 2002 December 1; 20(23): 4508-16 0732-183X
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Phase II neoadjuvant trial of paclitaxel by 96-hour continuous infusion (CIVI) in combination with cisplatin followed by chest radiotherapy for patients with stage III non-small-cell lung cancer. Author(s): Medicine Branch, Division of Clinical Sciences, National Cancer Institute (NCI)/National Naval Medical Center, NNMC, Bethesda, Maryland, USA. Source: Breathnach, O S Kasturi, V Kaye, F Herscher, L Georgiadis, M S Edison, M Schuler, B S Pizzella, P Steinberg, S M O'Neil, K Johnson, Bruce E Am-J-Clin-Oncol. 2002 June; 25(3): 269-73 0277-3732
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Phase II study of docetaxel and cisplatin combination chemotherapy in metastatic or unresectable localized non-small-cell lung cancer. Author(s): Department of Internal Medicine, Korea University, College of Medicine, Seoul, Korea. Source: Kim, Y H Kim, J S Choi, Y H In, K H Park, H S Hong, D S Jeong, T J Lee, Y Y Nam, E Lee, S N Lee, K S Kim, H K Int-J-Clin-Oncol. 2002 April; 7(2): 114-9 1341-9625
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Phase III randomized trial comparing three platinum-based doublets in advanced non-small-cell lung cancer. Author(s): Department of Clinical and Biological Sciences, University of Torino, Turin.
[email protected] Source: Scagliotti, G V De Marinis, F Rinaldi, M Crino, L Gridelli, C Ricci, S Matano, E Boni, C Marangolo, M Failla, G Altavilla, G Adamo, V Ceribelli, A Clerici, M Di Costanzo, F Frontini, L Tonato, M J-Clin-Oncol. 2002 November 1; 20(21): 4285-91 0732183X
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Platinum drugs in the treatment of non-small-cell lung cancer. Author(s): AstraZeneca, Mereside, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK. Source: Cosaert, J Quoix, E Br-J-Cancer. 2002 October 7; 87(8): 825-33 0007-0920
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Randomised phase III trial of irinotecan combined with cisplatin for advanced nonsmall-cell lung cancer. Author(s): Department of Clinical Oncology, Osaka City General Hospital, Osaka, Japan.
[email protected] Source: Negoro, S Masuda, N Takada, Y Sugiura, T Kudoh, S Katakami, N Ariyoshi, Y Ohashi, Y Niitani, H Fukuoka, M Br-J-Cancer. 2003 February 10; 88(3): 335-41 0007-0920
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): University of Chicago Medical Center and Cancer and Leukemia Group B, Chicago, IL, USA.
[email protected] Source: Vokes, E E Herndon, J E 2nd Crawford, J Leopold, K A Perry, M C Miller, A A Green, M R J-Clin-Oncol. 2002 October 15; 20(20): 4191-8 0732-183X
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Real-time polymerase chain reaction monitoring of epithelial cell adhesion moleculeinduced T-cell stimulation in patients with lung cancer and healthy individuals using LightCycler technology. Author(s): Division of Oncology, Department of Internal Medicine, University Hospital Zurich, Ramistrasse 100, CH-8091 Zurich, Switzerland.
[email protected] Source: TroJanuary, A Urosevic, M Dummer, R Nestle, F O Stahel, R A J-Immunother. 2002 May-June; 25(3): 264-8 1524-9557
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Recombinant human interleukin-3 administered concomitantly with chemotherapy in patients with relapsed small cell lung cancer. Author(s): Department of Pulmonology, University Hospital, Free University of Amsterdam, The Netherlands. Source: Biesma, B van Kralingen, K W van Leen, R W Koster, M C Postmus, P E J-ExpTher-Oncol. 2002 Jan-February; 2(1): 47-52 1359-4117
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Risk factors for lung cancer among Canadian women who have never smoked. Author(s): Centre for Chronic Disease Prevention and Control, Population and Public Health Brance, Health Canada, Ottawa, Ont. Source: Hu, J Mao, Y Dryer, D White, K Cancer-Detect-Prevolume 2002; 26(2): 129-38 0361-090X
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Salvage chemotherapy with the gemcitabine/docetaxel combination in non-small cell lung cancer: an overview of recent phase II studies. Author(s): Department of Medicine, Medical Oncology Unit, Helena-Venizelou Hospital, Athens, Greece.
[email protected] Source: Kosmas, C Tsavaris, N Kalofonos, H P Med-Sci-Monit. 2002 June; 8(6): PI58-63 1234-1010
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Second-line chemotherapy with irinotecan and vinorelbine in stage IIIB and IV nonsmall-cell lung cancer: a phase II study. Author(s): Department of Oncology, Clinica Universitaria de Navarra, University of Navarra, Spain. Source: Gonzalez Cao, M Aramendia, J M Salgado, E Aristu, J Martinez Monje, R Algarra, S M Ordonez, J M Brugarolas, A Am-J-Clin-Oncol. 2002 October; 25(5): 480-4 0277-3732
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Selective oral epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 is generally well-tolerated and has activity in non-small-cell lung cancer and other solid tumors: results of a phase I trial. Author(s): Department of Thoracic/Head and Neck Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
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Source: Herbst, R S Maddox, A M Rothenberg, M L Small, E J Rubin, E H Baselga, J Rojo, F Hong, W K Swaisland, H Averbuch, S D Ochs, J LoRusso, P M J-Clin-Oncol. 2002 September 15; 20(18): 3815-25 0732-183X ·
Significant growth inhibition of human lung cancer cells both in vitro and in vivo by the combined use of a selective cyclooxygenase 2 inhibitor, JTE-522, and conventional anticancer agents. Author(s): Department of Internal Medicine, Aichi Cancer Center Hospital, Nagoya 4648681, Japan.
[email protected] Source: Hida, T Kozaki, K Ito, H Miyaishi, O Tatematsu, Y Suzuki, T Matsuo, K Sugiura, T Ogawa, M Takahashi, T Takahashi, T Clin-Cancer-Res. 2002 July; 8(7): 2443-7 10780432
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Slow metabolism and long half life of methadone in a patient with lung cancer and cirrhosis. Author(s): Pharmacie, Hopital Paul-Guiraud, 54, avenue de la Republique, 94806 Villejuif Cedex.
[email protected] Source: Beauverie, P Furlan, V Edel, Y A Ann-Med-Interne-(Paris). 2001 November; 152 Suppl 7: 50-2 0003-410X
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The case for the introduction of new chemotherapy agents in the treatment of advanced non small cell lung cancer in the wake of the findings of The National Institute of Clinical Excellence (NICE). Author(s): Lung Unit, The Royal Marsden Hospital, Sutton, Surrey, UK. Source: Waters, J S O'Brien, M E Br-J-Cancer. 2002 August 27; 87(5): 481-90 0007-0920
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The role of carotenoids on the risk of lung cancer. Author(s): Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. Source: Epstein, K R Semin-Oncol. 2003 February; 30(1): 86-93 0093-7754
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Tumor lysis syndrome in extensive-stage small-cell lung cancer. Author(s): Department of Radiation Oncology, MS 200, Hahnemann University Hospital, Broad and Vine Street, Philadelphia, PA 19102, USA. Source: Beriwal, S Singh, S Garcia Young, J A Am-J-Clin-Oncol. 2002 October; 25(5): 4745 0277-3732
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Vinorelbine and paclitaxel for locoregional advanced or metastatic non-small-cell lung cancer. Author(s): Grupo Oncologico Cooperativo del Sur (G.O.C.S.), Republica Argentina. Source: Perez, Juan E Machiavelli, Mario R Romero, Alberto O Romero Acuna, Luis A Dominguez, Maria E Fasce, Hebe Flores Acosta, Luis Marrone, Nora Romero Acuna, Juan M Langhi, Mario J Amato, Sonia Bologna, Fabrina Ortiz, Eduardo H Leone, Bernardo A Lacava, Juan A Vallejo, Carlos T Am-J-Clin-Oncol. 2002 August; 25(4): 383-7 0277-3732
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Vinorelbine in the treatment of non-small cell lung cancer. Author(s): Divisione di Oncologia Medica, Azienda Ospedaliera S.G.Moscati, Avellino, Italy.
[email protected] Source: Gridelli, C De Vivo, R Curr-Med-Chem. 2002 April; 9(8): 879-91 0929-8673
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ZD1839 (Iressa) in non-small cell lung cancer. Author(s): Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Herbst, R S Kies, M S Oncologist. 2002; 7 Suppl 4: 9-15 1083-7159
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ZD1839 (Iressa): for more than just non-small cell lung cancer. Author(s): Department of Medical Oncology, Christie Hospital NHS Trust, Manchester, United Kingdom.
[email protected] Source: Ranson, M Oncologist. 2002; 7 Suppl 4: 16-24 1083-7159
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: ·
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: ·
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDÒHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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The following is a specific Web list relating to lung cancer; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: ·
Vitamins Folic Acid Source: Healthnotes, Inc.; www.healthnotes.com Provitamin A Source: Integrative Medicine Communications; www.drkoop.com Vitamin A Source: Healthnotes, Inc.; www.healthnotes.com Vitamin A Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10066,00.html Vitamin B12 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin E Source: Healthnotes, Inc.; www.healthnotes.com
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Minerals Cisplatin Source: Healthnotes, Inc.; www.healthnotes.com Quercetin Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10053,00.html Selenium Source: Healthnotes, Inc.; www.healthnotes.com Selenium Source: Integrative Medicine Communications; www.drkoop.com Selenium Source: Prima Communications, Inc.www.personalhealthzone.com Selenium Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10055,00.html
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Food and Diet Arugula Source: Healthnotes, Inc.; www.healthnotes.com Asparagus Source: Healthnotes, Inc.; www.healthnotes.com Beets Source: Healthnotes, Inc.; www.healthnotes.com Bok Choy Source: Healthnotes, Inc.; www.healthnotes.com Broccoli Source: Healthnotes, Inc.; www.healthnotes.com Carrots Source: Healthnotes, Inc.; www.healthnotes.com Chicory Source: Healthnotes, Inc.; www.healthnotes.com Collards Source: Healthnotes, Inc.; www.healthnotes.com Dandelion Greens Source: Healthnotes, Inc.; www.healthnotes.com Endive Source: Healthnotes, Inc.; www.healthnotes.com Kale Source: Healthnotes, Inc.; www.healthnotes.com Kohlrabi Source: Healthnotes, Inc.; www.healthnotes.com Mustard Greens Source: Healthnotes, Inc.; www.healthnotes.com Spinach Source: Healthnotes, Inc.; www.healthnotes.com Summer Squash Source: Healthnotes, Inc.; www.healthnotes.com Sweet Peppers Source: Healthnotes, Inc.; www.healthnotes.com Sweet Potatoes Source: Healthnotes, Inc.; www.healthnotes.com
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Tomatoes Source: Healthnotes, Inc.; www.healthnotes.com Turnips Source: Healthnotes, Inc.; www.healthnotes.com Winter Squash Source: Healthnotes, Inc.; www.healthnotes.com Yams Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND LUNG CANCER Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to lung cancer. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to lung cancer and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “lung cancer” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to lung cancer: ·
“The guard dies, it does not surrender!” progress in the management of small-cell lung cancer? Author(s): Johnson DH. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 15; 20(24): 4618-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488404&dopt=Abstract
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18F-fluorodeoxyglucose positron emission tomography in small-cell lung cancer. Author(s): Zhao DS, Valdivia AY, Li Y, Blaufox MD. Source: Semin Nucl Med. 2002 October; 32(4): 272-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524651&dopt=Abstract
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A dose escalation study of docetaxel and oxaliplatin combination in patients with metastatic breast and non-small cell lung cancer.
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Author(s): Kouroussis C, Agelaki S, Mavroudis D, Kakolyris S, Androulakis N, Kalbakis K, Souglakos J, Mallas K, Bozionelou V, Pallis A, Adamtziki H, Georgoulias V. Source: Anticancer Res. 2003 January-February; 23(1B): 785-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680184&dopt=Abstract ·
A little to a lot or a lot to a little? An analysis of pneumonitis risk from dose-volume histogram parameters of the lung in patients with lung cancer treated with 3-D conformal radiotherapy. Author(s): Willner J, Jost A, Baier K, Flentje M. Source: Strahlentherapie Und Onkologie : Organ Der Deutschen Rontgengesellschaft. [et Al]. 2003 August; 179(8): 548-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509954&dopt=Abstract
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A multicenter phase II study of docetaxel and carboplatin combination as front-line treatment in advanced non-small cell lung cancer. Author(s): Giannakakis T, Kakolyris S, Theodoropoulos E, Kouroussis C, Michailakis E, Papadouris S, Tsitoura M, Kalbakis K, Souglakos J, Agelaki S, Vardakis N, Georgoulias V. Source: Anticancer Res. 2002 November-December; 22(6B): 3743-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552987&dopt=Abstract
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A multicenter phase II study of the efficacy and safety of docetaxel plus cisplatin in Asian chemonaive patients with metastatic or locally advanced non-small cell lung cancer. Author(s): Ho JC, Tan EH, Leong SS, Wang CH, Sun Y, Li R, Wahid MI, Jusuf A, Liao M, Guan Z, Handoyo P, Huang JS, Chan V, Luna G, Tsang KW, Lam WK; Asian-Pacific Collaborative Group. Source: Respiratory Medicine. 2003 July; 97(7): 796-803. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854629&dopt=Abstract
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A phase I study of carboplatin and docetaxel for advanced non-small cell lung cancer using the continual reassessment method. Author(s): Kasahara K, Myo S, Iwasa K, Kimura H, Shirasaki H, Yasuda U, Shibata K, Shintani H, Nishi K, Fujimura M, Nakao S. Source: Japanese Journal of Clinical Oncology. 2002 December; 32(12): 512-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578899&dopt=Abstract
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A phase I trial of weekly docetaxel and cisplatinum combined to concurrent hyperfractionated radiotherapy for non-small cell lung cancer and squamous cell carcinoma of head and neck. Author(s): Varveris H, Mazonakis M, Vlachaki M, Kachris S, Lyraraki E, Zoras O, Maris T, Froudarakis M, Velegrakis J, Perysinakis C, Damilakis J, Samonis G. Source: Oncol Rep. 2003 January-February; 10(1): 185-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12469168&dopt=Abstract
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A phase II study of bryostatin-1 and paclitaxel in patients with advanced non-small cell lung cancer. Author(s): Winegarden JD, Mauer AM, Gajewski TF, Hoffman PC, Krauss S, Rudin CM, Vokes EE. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 191-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581572&dopt=Abstract
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A phase II study of carboplatin and vinorelbine in patients with poor prognosis small cell lung cancer. Author(s): Mackay HJ, O'Brien M, Hill S, Lees SM, Thatcher N, Smith IE, Dunlop DJ. Source: Clin Oncol (R Coll Radiol). 2003 June; 15(4): 181-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846495&dopt=Abstract
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A phase II study of non-platinum based chemotherapy with paclitaxel and vinorelbine in non-small cell lung cancer. Author(s): Ginopoulos P, Kontomanolis E, Kardamakis D, Sougleri M, Rathosis S, Karana A, Christias H, Mandellos G. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38(2): 199-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399133&dopt=Abstract
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A phase II study of vinorelbine, mitomycin C and cisplatin chemotherapy for advanced non-small cell lung cancer. Author(s): Kwon MR, Jeong TY, Yuh YJ, Kim SR. Source: Korean J Intern Med. 2002 December; 17(4): 240-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12647638&dopt=Abstract
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A phase II study of weekly gemcitabine and paclitaxel in patients with previously untreated stage IIIb and IV non-small cell lung cancer. Author(s): Bhatia S, Hanna N, Ansari R, Pletcher W, Einhorn L, Ng E, Sandler A. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 73-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367796&dopt=Abstract
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A phase II trial of chemotherapy and surgery for non-small cell lung cancer patients with a synchronous solitary metastasis. Author(s): Downey RJ, Ng KK, Kris MG, Bains MS, Miller VA, Heelan R, Bilsky M, Ginsberg R, Rusch VW. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38(2): 193-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399132&dopt=Abstract
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A phase II trial of vinorelbine plus gemcitabine in previously untreated inoperable (stage IIIb/IV) non-small-cell lung cancer patients aged 80 or older. Author(s): Chen YM, Perng RP, Chen MC, Tsai CM, Ming-Liu J, Whang-Peng J.
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Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711125&dopt=Abstract ·
A phase III randomized evaluation of amifostine in stage IIIA/IIIB non-small cell lung cancer patients receiving concurrent carboplatin, paclitaxel, and radiation therapy followed by gemcitabine and cisplatin intensification: preliminary findings. Author(s): Senzer N. Source: Seminars in Oncology. 2002 December; 29(6 Suppl 19): 38-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12577242&dopt=Abstract
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A randomized trial comparing induction chemotherapy followed by surgery with surgery alone for patients with stage IIIA N2 non-small cell lung cancer (JCOG 9209). Author(s): Nagai K, Tsuchiya R, Mori T, Tada H, Ichinose Y, Koike T, Kato H; Lung Cancer Surgical Study Group of the Japan Clinical Oncology Group. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 February; 125(2): 25460. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12579093&dopt=Abstract
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A retrospective analysis of the outcome of patients who have received two prior chemotherapy regimens including platinum and docetaxel for recurrent non-smallcell lung cancer. Author(s): Massarelli E, Andre F, Liu DD, Lee JJ, Wolf M, Fandi A, Ochs J, Le Chevalier T, Fossella F, Herbst RS. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 55-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499095&dopt=Abstract
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Adaptive intrapatient dose escalation of cisplatin in combination with low-dose vp16 in patients with nonsmall cell lung cancer. Author(s): Schellens JH, Planting AS, van Zandwijk N, Ma J, Maliepaard M, van der Burg ME, de Boer-Dennert M, Brouwer E, van der Gaast A, van den Bent MJ, Verweij J. Source: British Journal of Cancer. 2003 March 24; 88(6): 814-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644815&dopt=Abstract
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Alpha-1-acid glycoprotein as an independent predictor for treatment effects and a prognostic factor of survival in patients with non-small cell lung cancer treated with docetaxel. Author(s): Bruno R, Olivares R, Berille J, Chaikin P, Vivier N, Hammershaimb L, Rhodes GR, Rigas JR. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 March; 9(3): 1077-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631610&dopt=Abstract
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An advance in small-cell lung cancer treatment--more or less. Author(s): Laskin J, Sandler A, Johnson DH.
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Source: Journal of the National Cancer Institute. 2003 August 6; 95(15): 1099-101. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902431&dopt=Abstract ·
Antiproliferative and chemopreventive effects of adlay seed on lung cancer in vitro and in vivo. Author(s): Chang HC, Huang YC, Hung WC. Source: Journal of Agricultural and Food Chemistry. 2003 June 4; 51(12): 3656-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769541&dopt=Abstract
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Association between mitotic spindle checkpoint impairment and susceptibility to the induction of apoptosis by anti-microtubule agents in human lung cancers. Author(s): Masuda A, Maeno K, Nakagawa T, Saito H, Takahashi T. Source: American Journal of Pathology. 2003 September; 163(3): 1109-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937152&dopt=Abstract
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Bcl-2 and bax expression in advanced non-small cell lung cancer: lack of correlation with chemotherapy response or survival in patients treated with docetaxel plus vinorelbine. Author(s): Krug LM, Miller VA, Filippa DA, Venkatraman E, Ng KK, Kris MG. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 139-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581565&dopt=Abstract
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Beta-carotene and lung cancer: a lesson for future chemoprevention investigations? Author(s): Greenwald P. Source: Journal of the National Cancer Institute. 2003 January 1; 95(1): E1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509411&dopt=Abstract
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Breathlessness clinics within specialist palliative care settings can improve the quality of life and functional capacity of patients with lung cancer. Author(s): Hately J, Laurence V, Scott A, Baker R, Thomas P. Source: Palliative Medicine. 2003 July; 17(5): 410-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882259&dopt=Abstract
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Camptothecin and taxane regimens for small-cell lung cancer. Author(s): Kwong MS, Bleickardt E, Murren JR. Source: Oncology (Huntingt). 2002 September; 16(9 Suppl 9): 33-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12375799&dopt=Abstract
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Camptothecin induces urokinase-type plasminogen activator gene-expression in human RC-K8 malignant lymphoma and H69 small cell lung cancer cells. Author(s): Shibakura M, Niiya K, Kiguchi T, Nakata Y, Tanimoto M.
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Source: Acta Medica Okayama. 2002 October; 56(5): 223-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530505&dopt=Abstract ·
Camptothecins and lung cancer: improved delivery systems by aerosol. Author(s): Koshkina NV, Waldrep JC, Knight V. Source: Current Cancer Drug Targets. 2003 August; 3(4): 251-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871056&dopt=Abstract
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Carboplatin and paclitaxol (Taxol) as an induction regimen for patients with biopsyproven stage IIIA N2 non-small cell lung cancer. an EORTC phase II study (EORTC 08958). Author(s): O'Brien ME, Splinter T, Smit EF, Biesma B, Krzakowski M, Tjan-Heijnen VC, Van Bochove A, Stigt J, Smid-Geirnaerdt MJ, Debruyne C, Legrand C, Giaccone G; EORTC Lung Cancer Group. Source: European Journal of Cancer (Oxford, England : 1990). 2003 July; 39(10): 1416-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826045&dopt=Abstract
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Carboplatin plus vinorelbine with concomitant radiation therapy in advanced nonsmall cell lung cancer: a phase I study. Author(s): Hoffman PC, Cohen EE, Masters GA, Haraf DJ, Mauer AM, Rudin CM, Krauss SA, Huo D, Vokes EE. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 65-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367795&dopt=Abstract
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Celecoxib, a selective cyclo-oxygenase-2 inhibitor, enhances the response to preoperative paclitaxel and carboplatin in early-stage non-small-cell lung cancer. Author(s): Altorki NK, Keresztes RS, Port JL, Libby DM, Korst RJ, Flieder DB, Ferrara CA, Yankelevitz DF, Subbaramaiah K, Pasmantier MW, Dannenberg AJ. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2645-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860939&dopt=Abstract
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Chemotherapy for elderly patients with advanced non-small-cell lung cancer. Author(s): Bunn PA Jr, Lilenbaum R. Source: Journal of the National Cancer Institute. 2003 March 5; 95(5): 341-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618492&dopt=Abstract
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Chemotherapy for elderly patients with advanced non-small-cell lung cancer: the Multicenter Italian Lung Cancer in the Elderly Study (MILES) phase III randomized trial. Author(s): Gridelli C, Perrone F, Gallo C, Cigolari S, Rossi A, Piantedosi F, Barbera S, Ferrau F, Piazza E, Rosetti F, Clerici M, Bertetto O, Robbiati SF, Frontini L, Sacco C, Castiglione F, Favaretto A, Novello S, Migliorino MR, Gasparini G, Galetta D, Iaffaioli RV, Gebbia V; MILES Investigators.
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Source: Journal of the National Cancer Institute. 2003 March 5; 95(5): 362-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618501&dopt=Abstract ·
Chemotherapy for small cell lung cancer in patients over 80 years old. Author(s): Ueda H, Kuwahara M, Sakada T, Motohiro A. Source: Anticancer Res. 2002 November-December; 22(6B): 3629-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552967&dopt=Abstract
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Chemotherapy for small cell lung cancer. Author(s): Sandler AB. Source: Seminars in Oncology. 2003 February; 30(1): 9-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635086&dopt=Abstract
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Cisplatin and etoposide regimen is superior to cyclophosphamide, epirubicin, and vincristine regimen in small-cell lung cancer: results from a randomized phase III trial with 5 years' follow-up. Author(s): Sundstrom S, Bremnes RM, Kaasa S, Aasebo U, Hatlevoll R, Dahle R, Boye N, Wang M, Vigander T, Vilsvik J, Skovlund E, Hannisdal E, Aamdal S; Norwegian Lung Cancer Study Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 15; 20(24): 4665-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488411&dopt=Abstract
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Cisplatin plus gemcitabine versus a cisplatin-based triplet versus nonplatinum sequential doublets in advanced non-small-cell lung cancer: a Spanish Lung Cancer Group phase III randomized trial. Author(s): Alberola V, Camps C, Provencio M, Isla D, Rosell R, Vadell C, Bover I, RuizCasado A, Azagra P, Jimenez U, Gonzalez-Larriba JL, Diz P, Cardenal F, Artal A, Carrato A, Morales S, Sanchez JJ, de las Penas R, Felip E, Lopez-Vivanco G; Spanish Lung Cancer Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 1; 21(17): 3207-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947054&dopt=Abstract
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Cisplatin plus vinorelbine as induction chemotherapy followed by surgery in the treatment of stage IIIB non-small cell lung cancer. Final results of a multicenter phase II study. Author(s): Cigolari S, Curcio C, Maiorino A, Sessa R, Cioffi A, Massimo M. Source: Anticancer Res. 2003 March-April; 23(2C): 1803-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820462&dopt=Abstract
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Cisplatin-etoposide alternating with topotecan in patients with extensive stage small cell lung cancer (SCLC). A multicenter phase II study. Author(s): Mavroudis D, Veslemes M, Kouroussis Ch, Tzanakis N, Ferdoutsis E,
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Toumbis M, Ziotopoulos P, Agelidou M, Tselepatiotis E, Kalbakis K, Souglakos J, Magkanas E, Samonis G, Georgoulias V; Hellenic Oncology Research Group. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 59-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367794&dopt=Abstract ·
Combination chemotherapy with gemcitabine and vinorelbine in the treatment of patients with relapsed or refractory small cell lung cancer: a phase II trial of the Minnie Pearl Cancer Research Network. Author(s): Hainsworth JD, Burris HA 3rd, Erland JB, Baker M, Scullin DC Jr, Shaffer DW, Greco FA; Minnie Pearl Cancer Research Network. Source: Cancer Investigation. 2003 April; 21(2): 193-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743984&dopt=Abstract
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Combination second-line chemotherapy with gemcitabine and docetaxel for recurrent non-small-cell lung cancer after platinum-containing chemotherapy: a phase I/II trial. Author(s): Niho S, Kubota K, Goto K, Ohmatsu H, Matsumoto T, Kakinuma R, Nishiwaki Y. Source: Cancer Chemotherapy and Pharmacology. 2003 July; 52(1): 19-24. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712259&dopt=Abstract
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Comment on “A pilot trial of G3139, a bcl-2 antisense oligonucleotide, and paclitaxel in patients with chemorefractory small-cell lung cancer”, by C. M. Rudin et al. (Ann Oncol 2002; 13: 539-545). Author(s): Gautschi O, Zangemeister-Wittke U, Stahel RA. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 January; 14(1): 170. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488311&dopt=Abstract
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Comparing whole body 18F-2-deoxyglucose positron emission tomography and technetium-99m methylene diophosphate bone scan to detect bone metastases in patients with non-small cell lung cancer. Author(s): Hsia TC, Shen YY, Yen RF, Kao CH, Changlai SP. Source: Neoplasma. 2002; 49(4): 267-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12382027&dopt=Abstract
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Concomitant weekly docetaxel, cisplatin and radiation therapy in locally advanced non-small cell lung cancer: a dose finding study. Author(s): Mudad R, Ramsey M, Kovitz K, Curiel TJ, Hartz R, Nedzi LL, Weiner RS, Zakris EL. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 173-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581570&dopt=Abstract
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Concurrent two-dimensional radiotherapy and weekly docetaxel in the treatment of stage III non-small cell lung cancer: a good local response but no good survival due to radiation pneumonitis. Author(s): Onishi H, Kuriyama K, Yamaguchi M, Komiyama T, Tanaka S, Araki T, Nishikawa K, Ishihara H. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660011&dopt=Abstract
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Conservation of the class I beta-tubulin gene in human populations and lack of mutations in lung cancers and paclitaxel-resistant ovarian cancers. Author(s): Sale S, Sung R, Shen P, Yu K, Wang Y, Duran GE, Kim JH, Fojo T, Oefner PJ, Sikic BI. Source: Molecular Cancer Therapeutics. 2002 January; 1(3): 215-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12467216&dopt=Abstract
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Consolidation docetaxel after concurrent chemoradiotherapy in stage IIIB non-smallcell lung cancer: phase II Southwest Oncology Group Study S9504. Author(s): Gandara DR, Chansky K, Albain KS, Leigh BR, Gaspar LE, Lara PN Jr, Burris H, Gumerlock P, Kuebler JP, Bearden JD 3rd, Crowley J, Livingston R; Southwest Oncology Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 15; 21(10): 2004-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743155&dopt=Abstract
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Current role of irinotecan in the treatment of non-small-cell lung cancer. Author(s): Kelly K. Source: Oncology (Huntingt). 2002 September; 16(9): 1153-62, 1165; Discussion 1165-6 Passim. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12380945&dopt=Abstract
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DNA repair rate and etoposide (VP16) resistance of tumor cell subpopulations derived from a single human small cell lung cancer. Author(s): Hansen LT, Lundin C, Helleday T, Poulsen HS, Sorensen CS, Petersen LN, Spang-Thomsen M. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 157-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711116&dopt=Abstract
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Do age and comorbidity impact treatment allocation and outcomes in limited stage small-cell lung cancer? a community-based population analysis. Author(s): Ludbrook JJ, Truong PT, MacNeil MV, Lesperance M, Webber A, Joe H, Martins H, Lim J.
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Source: International Journal of Radiation Oncology, Biology, Physics. 2003 April 1; 55(5): 1321-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654444&dopt=Abstract ·
Docetaxel as neoadjuvant therapy for radically treatable stage III non-small-cell lung cancer: a multinational randomised phase III study. Author(s): Mattson KV, Abratt RP, ten Velde G, Krofta K. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 January; 14(1): 116-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488303&dopt=Abstract
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Docetaxel as second-line chemotherapy for advanced non-small cell lung cancer. Author(s): Thongprasert S, Cheewakriangkrai R, Napapan S. Source: J Med Assoc Thai. 2002 December; 85(12): 1296-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678167&dopt=Abstract
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Docetaxel in non-small cell lung cancer: a review. Author(s): Davies AM, Lara PN Jr, Mack PC, Gandara DR. Source: Expert Opinion on Pharmacotherapy. 2003 April; 4(4): 553-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12667118&dopt=Abstract
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Dose-dense therapy with a novel irinotecan regimen for small-cell lung cancer. Author(s): Johnson FM, Kurie JM, Peeples BO, Pisters KM, Fossella FV, Papadimitrakopoulou VA, Blumenschein GR, Komaki R, Glisson BS. Source: Oncology (Huntingt). 2003 July; 17(7 Suppl 7): 17-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886869&dopt=Abstract
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Dose-response relationship between probability of pathologic tumor control and glucose metabolic rate measured with FDG PET after preoperative chemoradiotherapy in locally advanced non-small-cell lung cancer. Author(s): Choi NC, Fischman AJ, Niemierko A, Ryu JS, Lynch T, Wain J, Wright C, Fidias P, Mathisen D. Source: International Journal of Radiation Oncology, Biology, Physics. 2002 November 15; 54(4): 1024-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419428&dopt=Abstract
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Dramatic effect of ZD1839 ('Iressa') in a patient with advanced non-small-cell lung cancer and poor performance status. Author(s): Fujiwara K, Kiura K, Ueoka H, Tabata M, Hamasaki S, Tanimoto M. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 73-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660009&dopt=Abstract
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Drugs for preventing lung cancer in healthy people. Author(s): Caraballoso M, Sacristan M, Serra C, Bonfill X. Source: Cochrane Database Syst Rev. 2003; (2): Cd002141. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804424&dopt=Abstract
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Early change in patient-reported health during lung cancer chemotherapy predicts clinical outcomes beyond those predicted by baseline report: results from Eastern Cooperative Oncology Group Study 5592. Author(s): Eton DT, Fairclough DL, Cella D, Yount SE, Bonomi P, Johnson DH; Eastern Cooperative Oncology Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 15; 21(8): 1536-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697878&dopt=Abstract
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Early tandem high-dose ifosfamide, carboplatin, etoposide therapy with stem cell rescue for small-cell lung cancer: brief report on the results of a phase-I/II trial. Author(s): Oelmann E, Thomas M, Serve H, Kienast J, Zuhlsdorf M, Mohr M, Klinke F, Dolken G, Macha H, Schmidt EW, Berdel WE. Source: Oncology. 2002; 63(3): 248-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381904&dopt=Abstract
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Economic evaluation of antibiotic prophylaxis in small-cell lung cancer patients receiving chemotherapy: an EORTC double-blind placebo-controlled phase III study (08923). Author(s): Tjan-Heijnen VC, Caleo S, Postmus PE, Ardizzoni A, Burghouts JT, Buccholz E, Biesma B, Gorlia T, Crott R, Giaccone G, Debruyne C, Manegold C; European Organisation for Research Treatment of Cancer-Lung Cancer Group and Health Economics Unit. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 February; 14(2): 248-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562652&dopt=Abstract
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Effect of amifostine on toxicities associated with radiochemotherapy in patients with locally advanced non-small-cell lung cancer. Author(s): Antonadou D, Throuvalas N, Petridis A, Bolanos N, Sagriotis A, Synodinou M. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2): 402-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12957251&dopt=Abstract
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Effects of radiotherapy and chemotherapy on lung function in patients with nonsmall-cell lung cancer. Author(s): Gopal R, Starkschall G, Tucker SL, Cox JD, Liao Z, Hanus M, Kelly JF, Stevens CW, Komaki R.
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Source: International Journal of Radiation Oncology, Biology, Physics. 2003 May 1; 56(1): 114-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694829&dopt=Abstract ·
Efficacy of modified regimen with attenuated doses of paclitaxel plus carboplatin combination chemotherapy in elderly and/or weak patients with advanced non-small cell lung cancer. Author(s): Choi IS, Kim BS, Park SR, Lee SY, Kim do Y, Kim JH, Lee SH, Kim TY, Heo DS, Bang YJ, Kim NK. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 99-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499101&dopt=Abstract
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End-of-life care in patients with lung cancer. Author(s): Griffin JP, Nelson JE, Koch KA, Niell HB, Ackerman TF, Thompson M, Cole FH Jr; American College of Chest Physicians. Source: Chest. 2003 January; 123(1 Suppl): 312S-331S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527587&dopt=Abstract
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Epiphora induced by intermittent docetaxel (taxotere) in patients with non-small cell lung cancer. Author(s): Spell DW, Estephan FF, Lin JT, Jones DV Jr. Source: Cancer Investigation. 2003; 21(4): 550-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14533445&dopt=Abstract
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Fatal pulmonary fibrosis associated with induction chemotherapy with carboplatin and vinorelbine followed by CHART radiotherapy for locally advanced non-small cell lung cancer. Author(s): Kirkbride P, Hatton M, Lorigan P, Joyce P, Fisher P. Source: Clin Oncol (R Coll Radiol). 2002 October; 14(5): 361-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555874&dopt=Abstract
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Feasibility of combination chemotherapy with cisplatin and etoposide for haemodialysis patients with lung cancer. Author(s): Watanabe R, Takiguchi Y, Moriya T, Oda S, Kurosu K, Tanabe N, Tatsumi K, Nagao K, Kuriyama T. Source: British Journal of Cancer. 2003 January 13; 88(1): 25-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556954&dopt=Abstract
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Fractionated administration of irinotecan and cisplatin for treatment of extensivedisease small-cell lung cancer: a phase II study. Author(s): Takigawa N, Fujiwara K, Ueoka H, Kiura K, Tabata M, Hiraki A, Shibayama T, Segawa Y, Kamei H, Hiraki S, Tanimoto M, Harada M.
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Source: Anticancer Res. 2003 January-February; 23(1B): 557-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680145&dopt=Abstract ·
Front-line paclitaxel/cisplatin-based chemotherapy in brain metastases from nonsmall-cell lung cancer. Author(s): Cortes J, Rodriguez J, Aramendia JM, Salgado E, Gurpide A, Garcia-Foncillas J, Aristu JJ, Claver A, Bosch A, Lopez-Picazo JM, Martin-Algarra S, Brugarolas A, Calvo E. Source: Oncology. 2003; 64(1): 28-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12457029&dopt=Abstract
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Fruits and vegetables are associated with lower lung cancer risk only in the placebo arm of the beta-carotene and retinol efficacy trial (CARET). Author(s): Neuhouser ML, Patterson RE, Thornquist MD, Omenn GS, King IB, Goodman GE. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2003 April; 12(4): 350-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692110&dopt=Abstract
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Gemcitabine and docetaxel every 2 weeks in advanced non-small cell lung cancer: a phase II study of the Gruppo Oncologico Italia Meridionale. Author(s): Galetta D, Gebbia V, Giotta F, Durini E, Romito S, Borsellino N, Cazzato C, Pezzella G, Colucci G. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367797&dopt=Abstract
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Gemcitabine and vinorelbine followed by docetaxel in patients with advanced nonsmall-cell lung cancer: a multi-institutional phase II trial of nonplatinum sequential triplet combination chemotherapy (JMTO LC00-02). Author(s): Hosoe S, Komuta K, Shibata K, Harada H, Iwamoto Y, Ohsaki Y, Morioka T, Origasa H, Fukushima M, Furuse K, Kawahara M. Source: British Journal of Cancer. 2003 February 10; 88(3): 342-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569374&dopt=Abstract
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Gemcitabine pharmacokinetics and interaction with paclitaxel in patients with advanced non-small-cell lung cancer. Author(s): Shord SS, Faucette SR, Gillenwater HH, Pescatore SL, Hawke RL, Socinski MA, Lindley C. Source: Cancer Chemotherapy and Pharmacology. 2003 April; 51(4): 328-36. Epub 2003 March 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721761&dopt=Abstract
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Gemcitabine plus vinorelbine compared with cisplatin plus vinorelbine or cisplatin plus gemcitabine for advanced non-small-cell lung cancer: a phase III trial of the Italian GEMVIN Investigators and the National Cancer Institute of Canada Clinical Trials Group. Author(s): Gridelli C, Gallo C, Shepherd FA, Illiano A, Piantedosi F, Robbiati SF, Manzione L, Barbera S, Frontini L, Veltri E, Findlay B, Cigolari S, Myers R, Ianniello GP, Gebbia V, Gasparini G, Fava S, Hirsh V, Bezjak A, Seymour L, Perrone F. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3025-34. Epub 2003 July 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837810&dopt=Abstract
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Gemcitabine, cisplatin and vinorelbine as induction chemotherapy followed by radical therapy in stage III non-small-cell lung cancer: a multicentre study of galicianlung-cancer-group. Author(s): Leon L, Cueva-Banuelos JF, Huidobro G, Firvida JL, Amenedo M, Lazaro M, Romero C, Estevez SV, Baron FJ, Grande C, Garcia Mata J, Gonzalez A, Castellanos J, Gomez A, Caeiro M, Rodriguez MR, Casal J; Galician Lung Cancer Group. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 215-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711124&dopt=Abstract
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GL331 inhibits HIF-1alpha expression in a lung cancer model. Author(s): Chang H, Shyu KG, Lee CC, Tsai SC, Wang BW, Hsien Lee Y, Lin S. Source: Biochemical and Biophysical Research Communications. 2003 February 28; 302(1): 95-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12593853&dopt=Abstract
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GLOB-1: a prospective randomised clinical phase III trial comparing vinorelbinecisplatin with vinorelbine-ifosfamide-cisplatin in metastatic non-small-cell lung cancer patients. Author(s): Souquet PJ, Tan EH, Rodrigues Pereira J, Van Klaveren R, Price A, Gatzemeier U, Jaworski M, Burillon JP, Aubert D. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 December; 13(12): 1853-61. Erratum In: Ann Oncol. 2003 February; 14(2): 347. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453852&dopt=Abstract
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In regard to hyperfractionation for non-small-cell lung cancer: fire, ready, aim! Author(s): Beitler JJ. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 April 1; 55(5): 1460; Author Reply 1460-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654462&dopt=Abstract
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In vivo assessment of tumor hypoxia in lung cancer with 60Cu-ATSM. Author(s): Dehdashti F, Mintun MA, Lewis JS, Bradley J, Govindan R, Laforest R, Welch MJ, Siegel BA.
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Source: European Journal of Nuclear Medicine and Molecular Imaging. 2003 June; 30(6): 844-50. Epub 2003 April 12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692685&dopt=Abstract ·
Influence of cisplatin-use, age, performance status and duration of chemotherapy on symptom control in advanced non-small cell lung cancer: detailed symptom analysis of a randomised study comparing cisplatin-vindesine to gemcitabine. Author(s): Vansteenkiste J, Vandebroek J, Nackaerts K, Dooms C, Galdermans D, Bosquee L, Delobbe A, Deschepper K, Van Kerckhoven W, Vandeurzen K, Deman R, D'Odemont JP, Siemons L, Van den Brande P, Dams N; Leuven Lung Cancer Group. Source: Lung Cancer (Amsterdam, Netherlands). 2003 May; 40(2): 191-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711121&dopt=Abstract
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Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy. Author(s): Krystal GW, Sulanke G, Litz J. Source: Molecular Cancer Therapeutics. 2002 September; 1(11): 913-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481412&dopt=Abstract
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Intraoperative radioguided sentinel lymph node biopsy in non-small cell lung cancer. Author(s): Melfi FM, Chella A, Menconi GF, Givigliano F, Boni G, Mariani G, Sbragia P, Angeletti CA. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2003 February; 23(2): 214-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559345&dopt=Abstract
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Invasive aspergillosis mimicking stage IIIA non-small-cell lung cancer on FDG positron emission tomography. Author(s): Wilkinson MD, Fulham MJ, McCaughan BC, Constable CJ. Source: Clinical Nuclear Medicine. 2003 March; 28(3): 234-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592137&dopt=Abstract
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Irinotecan and carboplatin in metastatic or recurrent non-small-cell lung cancer. Author(s): Govindan R, Read W, Faust J, Mc Leod H. Source: Oncology (Huntingt). 2003 July; 17(7 Suppl 7): 27-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886871&dopt=Abstract
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Irinotecan and vinorelbine in patients with non-small cell lung cancer previously treated with platinum-based chemotherapy. A phase II study of the Hellenic Cooperative Oncology Group. Author(s): Pectasides D, Fountzilas G, Rigopoulos A, Bountouroglou NG, Koutras A, Glotsos J, Onyenadum A, Makatsoris T, Kalofonos HP.
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Source: Anticancer Res. 2002 November-December; 22(6B): 3501-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552946&dopt=Abstract ·
Irinotecan in combination with radiation therapy for small-cell and non-small-cell lung cancer. Author(s): Wu HG, Choy H. Source: Oncology (Huntingt). 2002 September; 16(9 Suppl 9): 13-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12375796&dopt=Abstract
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Irinotecan plus cisplatin in small-cell lung cancer. Author(s): Sandler A. Source: Oncology (Huntingt). 2002 September; 16(9 Suppl 9): 39-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12375800&dopt=Abstract
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Irinotecan, cisplatin/carboplatin, and COX-2 inhibition in small-cell lung cancer. Author(s): Natale RB. Source: Oncology (Huntingt). 2003 July; 17(7 Suppl 7): 22-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886870&dopt=Abstract
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Is cisplatin still the best platinum compound in non-small-cell lung cancer? Author(s): Soria JC, Le Chevalier T. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 October; 13(10): 1515-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377638&dopt=Abstract
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Limited stage small cell lung cancer: treatment and therapy. Author(s): Turrisi AT 3rd. Source: Curr Treat Options Oncol. 2003 February; 4(1): 61-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525280&dopt=Abstract
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Low-dose weekly paclitaxel as second-line treatment for advanced non-small cell lung cancer: a phase II study. Author(s): Juan O, Albert A, Ordono F, Casany R, Caranana V, Campos JM, Alberola V. Source: Japanese Journal of Clinical Oncology. 2002 November; 32(11): 449-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499416&dopt=Abstract
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Lung cancer. Practice organization. Author(s): Alberts WM, Bepler G, Hazelton T, Ruckdeschel JC, Williams JH Jr; American College of Chest Physicians. Source: Chest. 2003 January; 123(1 Suppl): 332S-337S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527588&dopt=Abstract
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Mediastinal lymph node clearance after docetaxel-cisplatin neoadjuvant chemotherapy is prognostic of survival in patients with stage IIIA pN2 non-small-cell lung cancer: a multicenter phase II trial. Author(s): Betticher DC, Hsu Schmitz SF, Totsch M, Hansen E, Joss C, von Briel C, Schmid RA, Pless M, Habicht J, Roth AD, Spiliopoulos A, Stahel R, Weder W, Stupp R, Egli F, Furrer M, Honegger H, Wernli M, Cerny T, Ris HB. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1752-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721251&dopt=Abstract
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Mediastinal lymph node involvement in non-small cell lung cancer: evaluation with 99mTc-tetrofosmin SPECT and comparison with CT. Author(s): Schillaci O, Spanu A, Scopinaro F, Monteleone F, Solinas ME, Volpino P, Pirina P, Marongiu P, Cangemi V, Madeddu G. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 August; 44(8): 1219-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902410&dopt=Abstract
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Mediastinal lymph node involvement in potentially resectable lung cancer: comparison of CT, positron emission tomography, and endoscopic ultrasonography with and without fine-needle aspiration. Author(s): Fritscher-Ravens A, Bohuslavizki KH, Brandt L, Bobrowski C, Lund C, Knofel WT, Pforte A. Source: Chest. 2003 February; 123(2): 442-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576364&dopt=Abstract
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Methods to monitor response to chemotherapy in non-small cell lung cancer with 18F-FDG PET. Author(s): Hoekstra CJ, Hoekstra OS, Stroobants SG, Vansteenkiste J, Nuyts J, Smit EF, Boers M, Twisk JW, Lammertsma AA. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2002 October; 43(10): 1304-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368367&dopt=Abstract
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Mitochondrial damage prior to apoptosis in furanonaphthoquinone treated lung cancer cells. Author(s): Simamura E, Hirai K, Shimada H, Pan J, Koyama J. Source: Cancer Detection and Prevention. 2003; 27(1): 5-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12600411&dopt=Abstract
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Modification of lung cancer susceptibility by green tea extract as measured by the comet assay. Author(s): Zhang H, Spitz MR, Tomlinson GE, Schabath MB, Minna JD, Wu X.
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Source: Cancer Detection and Prevention. 2002; 26(6): 411-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507225&dopt=Abstract ·
Molecular markers and targeted therapy with novel agents: prospects in the treatment of non-small cell lung cancer. Author(s): Rosell R, Fossella F, Milas L; Spanish Lung Cancer Group. Source: Lung Cancer (Amsterdam, Netherlands). 2002 December; 38 Suppl 4: 43-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480194&dopt=Abstract
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Multicenter, randomized trial for stage IIIB or IV non-small-cell lung cancer using weekly paclitaxel and carboplatin followed by maintenance weekly paclitaxel or observation. Author(s): Belani CP, Barstis J, Perry MC, La Rocca RV, Nattam SR, Rinaldi D, Clark R, Mills GM. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2933-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885812&dopt=Abstract
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Neoadjuvant radiotherapy concurrent with weekly paclitaxel and carboplatin and followed by surgery in locally advanced non-small-cell lung cancer. Author(s): Kuten A, Anacak Y, Abdah-Bortnyak R, Chetver L, Zen Al Deen I, Daoud K, Nijem R, Billan S, Best L. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2003 April; 26(2): 184-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714893&dopt=Abstract
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Non-platinum gemcitabine combinations in non-small cell lung cancer. Author(s): Marx G, Harper P. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38 Suppl 2: S51-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431830&dopt=Abstract
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Outpatient intensive chemotherapy for small cell lung cancer: five years experience of modified 'ICE' ifosfamide carboplatin and etoposide. Author(s): Hand S, Baker J, Smith AP, Macbeth FR. Source: Clin Oncol (R Coll Radiol). 2002 October; 14(5): 367-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555875&dopt=Abstract
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P21 response to DNA damage induced by genistein and etoposide in human lung cancer cells. Author(s): Ding H, Duan W, Zhu WG, Ju R, Srinivasan K, Otterson GA, Villalona-Calero MA.
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Source: Biochemical and Biophysical Research Communications. 2003 June 13; 305(4): 950-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767922&dopt=Abstract ·
p53 status and its in vitro relationship to radiosensitivity and chemosensitivity in lung cancer. Author(s): Bergqvist M, Brattstrom D, Gullbo J, Hesselius P, Brodin O, Wagenius G. Source: Anticancer Res. 2003 March-April; 23(2B): 1207-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820372&dopt=Abstract
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Paclitaxel (taxol) and taxoid derivates for lung cancer treatment: potential for aerosol delivery. Author(s): Gautam A, Koshkina N. Source: Current Cancer Drug Targets. 2003 August; 3(4): 287-96. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871059&dopt=Abstract
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Patterns of failure in patients who had response-assessment by PET after radical radiotherapy for non-small cell lung cancer support the case for more intensive local therapy. Author(s): Mac Manus MP, Hicks R, Jane M, Andrew W, Danny R, Annette H, David BL. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2 Suppl): S167. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965403&dopt=Abstract
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PET scanning in lung cancer: current status and future directions. Author(s): Mac Manus MP, Hicks RJ. Source: Seminars in Surgical Oncology. 2003; 21(3): 149-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508847&dopt=Abstract
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PG490-mediated sensitization of lung cancer cells to Apo2L/TRAIL-induced apoptosis requires activation of ERK2. Author(s): Frese S, Pirnia F, Miescher D, Krajewski S, Borner MM, Reed JC, Schmid RA. Source: Oncogene. 2003 August 21; 22(35): 5427-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934102&dopt=Abstract
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Phase I and pharmacokinetic study of carboplatin and paclitaxel with a biweekly schedule in patients with advanced non-small-cell lung cancer. Author(s): Ichiki M, Gohara R, Fujiki R, Hoashi S, Rikimaru T, Aizawa H. Source: Cancer Chemotherapy and Pharmacology. 2003 July; 52(1): 67-72. Epub 2003 May 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743738&dopt=Abstract
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Phase I study of irinotecan and cisplatin with concurrent split-course radiotherapy in limited-disease small-cell lung cancer. Author(s): Oka M, Fukuda M, Kuba M, Ichiki M, Rikimaru T, Soda H, Tsurutani J, Nakamura Y, Kawabata S, Nakatomi K, Narasaki F, Nagashima S, Takatani H, Fukuda M, Kinoshita A, Kohno S. Source: European Journal of Cancer (Oxford, England : 1990). 2002 October; 38(15): 19982004. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376204&dopt=Abstract
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Phase I study of paclitaxel and topotecan for the first-line treatment of extensive-stage small cell lung cancer. Author(s): West W, Birch R, Schnell F, Hainsworth J, Tongol J, Campos L. Source: The Oncologist. 2003; 8(1): 76-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604734&dopt=Abstract
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Phase I trial of weekly docetaxel in elderly patients with non-small cell lung cancer. Author(s): Inoue A, Kunitoh H, Mori K, Nukiwa T, Fukuoka M, Saijo N. Source: Lung Cancer (Amsterdam, Netherlands). 2002 November; 38(2): 205-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399134&dopt=Abstract
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Phase I/II investigation of paclitaxel, ifosfamide and carboplatin for advanced nonsmall-cell lung cancer. Author(s): Mauer AM, Ansari RH, Hoffman PC, Krauss SA, Taber D, Tembe SA, Gabrys GT, Cotter T, Schumm LP, Szeto L, Vokes EE. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 May; 14(5): 722-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702526&dopt=Abstract
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Phase I/II study of docetaxel and cisplatin with concurrent thoracic radiation therapy for locally advanced non-small-cell lung cancer. Author(s): Kiura K, Ueoka H, Segawa Y, Tabata M, Kamei H, Takigawa N, Hiraki S, Watanabe Y, Bessho A, Eguchi K, Okimoto N, Harita S, Takemoto M, Hiraki Y, Harada M, Tanimoto M; Okayama Lung Cancer Study Group. Source: British Journal of Cancer. 2003 September 1; 89(5): 795-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942107&dopt=Abstract
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Phase I/II study of escalating doses of nedaplatin in combination with irinotecan for advanced non-small-cell lung cancer. Author(s): Oshita F, Yamada K, Kato Y, Ikehara M, Noda K, Tanaka G, Nomura I, Suzuki R, Saito H. Source: Cancer Chemotherapy and Pharmacology. 2003 July; 52(1): 73-8. Epub 2003 May 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750839&dopt=Abstract
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Phase I/II study of paclitaxel, gemcitabine and vinorelbine as first-line chemotherapy of non-small-cell lung cancer. Author(s): Lorusso V, Crucitta E, Panza N, Silvestris N, Guida M, Carpagnano F, Mancarella S, Sambiasi D, De Lena M. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 December; 13(12): 1862-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453853&dopt=Abstract
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Phase I/II trial of gemcitabine plus cisplatin and etoposide in patients with small-cell lung cancer. Author(s): De Marinis F, Migliorino MR, Paoluzzi L, Portalone L, Ariganello O, Cortesi E, Gamucci T, Gasperoni S, Cipri A, Martelli O, Nelli F; Foundation for Oncological Research. Source: Lung Cancer (Amsterdam, Netherlands). 2003 March; 39(3): 331-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12609572&dopt=Abstract
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Phase I/II trial of vinorelbine and divided-dose carboplatin in advanced non-small cell lung cancer. Author(s): Masters GA, Hahn EA, Shevrin DH, Kies MS. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581577&dopt=Abstract
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Phase I/II trial of weekly cisplatin, etoposide, and irinotecan chemotherapy for metastatic lung cancer: JCOG 9507. Author(s): Sekine I, Nishiwaki Y, Kakinuma R, Kubota K, Hojo F, Matsumoto T, Ohmatsu H, Goto K, Kodama T, Eguchi K, Shinkai T, Tamura T, Ohe Y, Kunitoh H, Yoshimura K, Saijo N. Source: British Journal of Cancer. 2003 March 24; 88(6): 808-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644814&dopt=Abstract
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Phase II and pharmacologic study of weekly oral paclitaxel plus cyclosporine in patients with advanced non-small-cell lung cancer. Author(s): Kruijtzer CM, Schellens JH, Mezger J, Scheulen ME, Keilholz U, Beijnen JH, Rosing H, Mathot RA, Marcus S, van Tinteren H, Baas P. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 1; 20(23): 4508-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454106&dopt=Abstract
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Phase II non-randomized study of three different sequences of docetaxel and vinorelbine in patients with advanced non-small cell lung cancer. Author(s): Sanchez JM, Balana C, Font A, Sanchez JJ, Manzano JL, Guillot M, Margeli M, Richardet M, Rosell R.
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Source: Lung Cancer (Amsterdam, Netherlands). 2002 December; 38(3): 309-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12445754&dopt=Abstract ·
Phase II study of carboplatin and 1-h intravenous etoposide and paclitaxel in a novel sequence as first-line treatment of patients with small-cell lung cancer. Author(s): Vieitez JM, Valladares M, Gracia M, Gonzalez-Baron M, Martin G, Mel JR, Rodriguez R, Constenla M, Gomez Aldavari JL, Dominguez S, Dorta J, Garcia-Giron C, Lopez R, Sevilla I, Esteban E, Anton LM, Pelaez I, Lopez E, Lacave AJ. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 77-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499098&dopt=Abstract
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Phase II study of cisplatin, ifosfamide, and irinotecan with rhG-CSF support in patients with stage IIIb and IV non-small-cell lung cancer. Author(s): Fujita A, Ohkubo T, Hoshino H, Takabatake H, Tagaki S, Sekine K, Abe S. Source: British Journal of Cancer. 2003 September 15; 89(6): 1008-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966417&dopt=Abstract
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Phase II study of docetaxel and gemcitabine combination chemotherapy in nonsmall-cell lung cancer patients failing previous chemotherapy. Author(s): Chen YM, Perng RP, Lin WC, Wu HW, Tsai CM, Whang-Peng J. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2002 October; 25(5): 509-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393994&dopt=Abstract
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Phase II study of docetaxel and ifosfamide combination chemotherapy in non-smallcell lung cancer patients failing previous chemotherapy with or without paclitaxel. Author(s): Chen YM, Shih JF, Lee CS, Chen MC, Lin WC, Tsai CM, Perng RP. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 209-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581575&dopt=Abstract
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Phase II study of irinotecan and carboplatin for advanced non-small cell lung cancer. Author(s): Takeda K, Takifuji N, Uejima H, Yoshimura N, Terakawa K, Negoro S. Source: Lung Cancer (Amsterdam, Netherlands). 2002 December; 38(3): 303-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12445753&dopt=Abstract
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Phase II study of irinotecan and carboplatin in patients with the refractory or relapsed small cell lung cancer. Author(s): Hirose T, Horichi N, Ohmori T, Ogura K, Hosaka T, Ando K, Ishida H, Noguchi H, Adachi M. Source: Lung Cancer (Amsterdam, Netherlands). 2003 June; 40(3): 333-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781433&dopt=Abstract
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Phase II study of irinotecan and ifosfamide in patients with advanced non-small cell lung cancer. Author(s): Ichiki M, Rikimaru T, Gohara R, Koga T, Kawayama T, Matunami M, Oshita Y, Kamimura T, Aizawa H. Source: Oncology. 2003; 64(4): 306-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759525&dopt=Abstract
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Phase II study of neoadjuvant chemotherapy in patients with surgically-proven, unresectable stage III non-small cell lung cancer. Author(s): Grossi F, Pennucci MC, Serrano J, Frola C, Mereu C, Scolaro T, Ratto GB, Tixi L, Ardizzoni A. Source: Anticancer Res. 2002 November-December; 22(6B): 3519-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552949&dopt=Abstract
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Phase II study of paclitaxel (Genaxol) and cisplatin combination in treating Chinese patients with advanced non-small cell lung cancer (NSCLC). Author(s): Chen CH, Chang WC, Lin MC, Hsu JW, Chao TY, Tsao TC. Source: Lung Cancer (Amsterdam, Netherlands). 2002 October; 38(1): 91-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12367799&dopt=Abstract
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Phase II study of Taxol combined With ifosfamide and carboplatin in the treatment of stage IIIb-IV non-small-cell lung cancer. Author(s): Zaniboni A, Ardizzoni A, De Marinis F, Portalone L, Boni C, Meriggi F, Cafferata MA, Ariganello O, Torri V, Neumaier CE, Rosso R. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2003 February; 26(1): 84-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576930&dopt=Abstract
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Phase II study of three-dimensional conformal radiotherapy and concurrent mitomycin-C, vinblastine, and cisplatin chemotherapy for Stage III locally advanced, unresectable, non-small-cell lung cancer. Author(s): Lee SW, Choi EK, Lee JS, Lee SD, Suh C, Kim SW, Kim WS, Ahn SD, Yi BY, Kim JH, Noh YJ, Kim SS, Koh Y, Kim DS, Kim WD. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 July 15; 56(4): 996-1004. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829135&dopt=Abstract
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Phase II study with vinorelbine and cisplatin in advanced non-small cell lung cancer after failure of previous chemotherapy. Author(s): Chen YM, Lee CS, Lin WC, Tsai CM, Perng RP. Source: J Chin Med Assoc. 2003 April; 66(4): 241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854877&dopt=Abstract
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Phase II trial of paclitaxel, ifosfamide, and carboplatin in extensive-stage small cell lung cancer. Author(s): Socinski MA, Neubauer MA, Olivares J, Ketchel S, Tynan M, Moore M, Lee JH, Davis K, Schell M, Garfield D. Source: Lung Cancer (Amsterdam, Netherlands). 2003 April; 40(1): 91-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660013&dopt=Abstract
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Phase III randomised trial comparing paclitaxel/carboplatin with paclitaxel/cisplatin in patients with advanced non-small-cell lung cancer: a cooperative multinational trial. Author(s): Rosell R, Gatzemeier U, Betticher DC, Keppler U, Macha HN, Pirker R, Berthet P, Breau JL, Lianes P, Nicholson M, Ardizzoni A, Chemaissani A, Bogaerts J, Gallant G. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 October; 13(10): 1539-49. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377641&dopt=Abstract
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Phase III randomized trial comparing three platinum-based doublets in advanced non-small-cell lung cancer. Author(s): Scagliotti GV, De Marinis F, Rinaldi M, Crino L, Gridelli C, Ricci S, Matano E, Boni C, Marangolo M, Failla G, Altavilla G, Adamo V, Ceribelli A, Clerici M, Di Costanzo F, Frontini L, Tonato M; Italian Lung Cancer Project. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 1; 20(21): 4285-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409326&dopt=Abstract
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Pilot trial of the epidermal growth factor receptor tyrosine kinase inhibitor gefitinib plus carboplatin and paclitaxel in patients with stage IIIB or IV non-small-cell lung cancer. Author(s): Miller VA, Johnson DH, Krug LM, Pizzo B, Tyson L, Perez W, Krozely P, Sandler A, Carbone D, Heelan RT, Kris MG, Smith R, Ochs J. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2094-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775734&dopt=Abstract
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Platinum drugs in the treatment of non-small-cell lung cancer. Author(s): Cosaert J, Quoix E. Source: British Journal of Cancer. 2002 October 7; 87(8): 825-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12373594&dopt=Abstract
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Platinum-based, leukocyte-depleting chemotherapy does not alter induced sputum markers of neutrophilic inflammation in COPD patients with unresectable non-small cell lung cancer. Author(s): Beeh KM, Beier J, Ernst M, Kornmann O, Buhl R.
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Source: Respiration; International Review of Thoracic Diseases. 2003 March-April; 70(2): 166-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740514&dopt=Abstract ·
Positron emission tomography (PET) and combined imaging modalities for staging lung cancer. Author(s): Scott WJ. Source: The Surgical Clinics of North America. 2002 June; 82(3): 477-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12371581&dopt=Abstract
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Positron emission tomography in lung cancer. Author(s): Shon IH, O'doherty MJ, Maisey MN. Source: Semin Nucl Med. 2002 October; 32(4): 240-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524650&dopt=Abstract
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Positron emission tomography in non-small-cell lung cancer: prediction of response to chemotherapy by quantitative assessment of glucose use. Author(s): Weber WA, Petersen V, Schmidt B, Tyndale-Hines L, Link T, Peschel C, Schwaiger M. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2651-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860940&dopt=Abstract
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Positron emission tomography is superior to computed tomography scanning for response-assessment after radical radiotherapy or chemoradiotherapy in patients with non-small-cell lung cancer. Author(s): Mac Manus MP, Hicks RJ, Matthews JP, McKenzie A, Rischin D, Salminen EK, Ball DL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 1; 21(7): 1285-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663716&dopt=Abstract
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Potential for reduced toxicity and dose escalation in the treatment of inoperable nonsmall-cell lung cancer: a comparison of intensity-modulated radiation therapy (IMRT), 3D conformal radiation, and elective nodal irradiation. Author(s): Grills IS, Yan D, Martinez AA, Vicini FA, Wong JW, Kestin LL. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 November 1; 57(3): 875-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14529795&dopt=Abstract
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Potentiation of the effect of paclitaxel and carboplatin by antioxidant mixture on human lung cancer h520 cells. Author(s): Pathak AK, Singh N, Khanna N, Reddy VG, Prasad KN, Kochupillai V.
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Source: Journal of the American College of Nutrition. 2002 October; 21(5): 416-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12356783&dopt=Abstract ·
Predicting chemotherapy response to paclitaxel-based therapy in advanced nonsmall-cell lung cancer with P-glycoprotein expression. Author(s): Yeh JJ, Hsu WH, Wang JJ, Ho ST, Kao A. Source: Respiration; International Review of Thoracic Diseases. 2003 January-February; 70(1): 32-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584388&dopt=Abstract
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Preliminary results of radiotherapy with or without weekly paclitaxel in locally advanced non-small cell lung cancer. Author(s): Cuneyt Ulutin H, Pak Y. Source: Journal of Cancer Research and Clinical Oncology. 2003 January; 129(1): 52-6. Epub 2003 January 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618901&dopt=Abstract
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Pretreatment clinical prognostic factors in patients with stage IV non-small cell lung cancer (NSCLC) treated with chemotherapy. Author(s): Jeremic B, Milicic B, Dagovic A, Aleksandrovic J, Nikolic N. Source: Journal of Cancer Research and Clinical Oncology. 2003 February; 129(2): 114-22. Epub 2003 March 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12669236&dopt=Abstract
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Pretreatment serum levels of matrix metalloproteinase-9 and vascular endothelial growth factor in non-small-cell lung cancer. Author(s): Laack E, Kohler A, Kugler C, Dierlamm T, Knuffmann C, Vohwinkel G, Niestroy A, Dahlmann N, Peters A, Berger J, Fiedler W, Hossfeld DK. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 October; 13(10): 1550-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377642&dopt=Abstract
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Prevention of lung cancer: summary of published evidence. Author(s): Kelley MJ, McCrory DC. Source: Chest. 2003 January; 123(1 Suppl): 50S-59S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527564&dopt=Abstract
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Preventive effect of Kampo medicine (Hangeshashin-to) against irinotecan-induced diarrhea in advanced non-small-cell lung cancer. Author(s): Mori K, Kondo T, Kamiyama Y, Kano Y, Tominaga K.
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Source: Cancer Chemotherapy and Pharmacology. 2003 May; 51(5): 403-6. Epub 2003 April 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687289&dopt=Abstract ·
Prognostic factors in Greek patients with small cell lung cancer (SCLC). A Hellenic Cooperative Oncology Group study. Author(s): Christodolou C, Pavlidis N, Samantas E, Fountzilas G, Kouvatseas G, Pagdatoglou K, Palamidas F, Nikolaidis C, Angelidou M, Kalofonos HP, Kosmidis P, Skarlos DV. Source: Anticancer Res. 2002 November-December; 22(6B): 3749-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552988&dopt=Abstract
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Prolonged administration of infusional cisplatin and oral etoposide in advanced nonsmall cell lung cancer. Author(s): Jazieh AR, Kyasa MJ, Muirhead MJ. Source: Anti-Cancer Drugs. 2002 September; 13(8): 815-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12394265&dopt=Abstract
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Prospective use of serial questionnaires to evaluate the therapeutic efficacy of 18Ffluorodeoxyglucose (FDG) positron emission tomography (PET) in suspected lung cancer. Author(s): Herder GJ, Van Tinteren H, Comans EF, Hoekstra OS, Teule GJ, Postmus PE, Joshi U, Smit EF. Source: Thorax. 2003 January; 58(1): 47-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12511720&dopt=Abstract
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Pulmonary function following high-dose radiotherapy of non-small-cell lung cancer. Author(s): De Jaeger K, Seppenwoolde Y, Boersma LJ, Muller SH, Baas P, Belderbos JS, Lebesque JV. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 April 1; 55(5): 1331-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654445&dopt=Abstract
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Radiation-induced apoptosis in human non-small-cell lung cancer cell lines is secondary to cell-cycle progression beyond the G2-phase checkpoint. Author(s): Stuschke M, Sak A, Wurm R, Sinn B, Wolf G, Stuben G, Budach V. Source: International Journal of Radiation Biology. 2002 September; 78(9): 807-19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428922&dopt=Abstract
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Randomised phase III trial of irinotecan combined with cisplatin for advanced nonsmall-cell lung cancer. Author(s): Negoro S, Masuda N, Takada Y, Sugiura T, Kudoh S, Katakami N, Ariyoshi Y, Ohashi Y, Niitani H, Fukuoka M; CPT-11 Lung Cancer Study Group West.
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Source: British Journal of Cancer. 2003 February 10; 88(3): 335-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569373&dopt=Abstract ·
Randomized double-blind trial of combined modality treatment with or without amifostine in unresectable stage III non-small-cell lung cancer. Author(s): Leong SS, Tan EH, Fong KW, Wilder-Smith E, Ong YK, Tai BC, Chew L, Lim SH, Wee J, Lee KM, Foo KF, Ang P, Ang PT. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1767-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721253&dopt=Abstract
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): Vokes EE, Herndon JE 2nd, Crawford J, Leopold KA, Perry MC, Miller AA, Green MR. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 October 15; 20(20): 4191-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377962&dopt=Abstract
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Randomized phase II study of cisplatin, irinotecan and etoposide combinations administered weekly or every 4 weeks for extensive small-cell lung cancer (JCOG9902-DI). Author(s): Sekine I, Nishiwaki Y, Noda K, Kudoh S, Fukuoka M, Mori K, Negoro S, Yokoyama A, Matsui K, Ohsaki Y, Nakano T, Saijo N; Japan Clinical Oncology Group (JCOG) Lung Cancer Study Group. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 May; 14(5): 709-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702524&dopt=Abstract
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Randomized phase III trial of paclitaxel, etoposide, and carboplatin versus carboplatin, etoposide, and vincristine in patients with small-cell lung cancer. Author(s): Reck M, von Pawel J, Macha HN, Kaukel E, Deppermann KM, Bonnet R, Ulm K, Hessler S, Gatzemeier U. Source: Journal of the National Cancer Institute. 2003 August 6; 95(15): 1118-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902441&dopt=Abstract
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Randomized study of adjuvant chemotherapy for completely resected stage I, II, or IIIA non-small-cell Lung cancer. Author(s): Scagliotti GV, Fossati R, Torri V, Crino L, Giaccone G, Silvano G, Martelli M, Clerici M, Cognetti F, Tonato M; Adjuvant Lung Project Italy/European Organisation for Research Treatment of Cancer-Lung Cancer Cooperative Group Investigators. Source: Journal of the National Cancer Institute. 2003 October 1; 95(19): 1453-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519751&dopt=Abstract
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Randomized, multinational, phase III study of docetaxel plus platinum combinations versus vinorelbine plus cisplatin for advanced non-small-cell lung cancer: the TAX 326 study group. Author(s): Fossella F, Pereira JR, von Pawel J, Pluzanska A, Gorbounova V, Kaukel E, Mattson KV, Ramlau R, Szczesna A, Fidias P, Millward M, Belani CP. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3016-24. Epub 2003 July 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837811&dopt=Abstract
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Recombinant human interleukin-3 administered concomitantly with chemotherapy in patients with relapsed small cell lung cancer. Author(s): Biesma B, van Kralingen KW, van Leen RW, Koster MC, Postmus PE. Source: Journal of Experimental Therapeutics & Oncology. 2002 January-February; 2(1): 47-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415620&dopt=Abstract
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Response to cisplatin-etoposide treatment and survival in patients with small-cell lung cancer in North Lebanon. Author(s): Kalaajieh WK. Source: Medical Principles and Practice : International Journal of the Kuwait University, Health Science Centre. 2003 April-June; 12(2): 117-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634468&dopt=Abstract
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Role of mycobacterium w as adjuvant treatment of lung cancer (non-small cell lung cancer). Author(s): Sur PK, Dastidar AG. Source: J Indian Med Assoc. 2003 February; 101(2): 118, 120. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841498&dopt=Abstract
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Safety and pharmacokinetic effects of TNP-470, an angiogenesis inhibitor, combined with paclitaxel in patients with solid tumors: evidence for activity in non-small-cell lung cancer. Author(s): Herbst RS, Madden TL, Tran HT, Blumenschein GR Jr, Meyers CA, Seabrooke LF, Khuri FR, Puduvalli VK, Allgood V, Fritsche HA Jr, Hinton L, Newman RA, Crane EA, Fossella FV, Dordal M, Goodin T, Hong WK. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 15; 20(22): 4440-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431966&dopt=Abstract
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Screening for early lung cancer with low-dose spiral computed tomography. Author(s): Diederich S. Source: Lancet. 2003 August 23; 362(9384): 588-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944053&dopt=Abstract
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Second-line chemotherapy with irinotecan and vinorelbine in stage IIIB and IV nonsmall-cell lung cancer: a phase II study. Author(s): Gonzalez Cao M, Aramendia JM, Salgado E, Aristu J, Martinez Monje R, Algarra SM, Ordonez JM, Brugarolas A. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2002 October; 25(5): 480-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393989&dopt=Abstract
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Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial. Author(s): Reid ME, Duffield-Lillico AJ, Garland L, Turnbull BW, Clark LC, Marshall JR. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 November; 11(11): 1285-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12433704&dopt=Abstract
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Sensitivity of non-small-cell lung cancer cell lines established from patients treated with prolonged infusions of Paclitaxel. Author(s): Fujishita T, Loda M, Turner RE, Gentler M, Kashii T, Breathnach OS, Johnson BE. Source: Oncology. 2003; 64(4): 399-406. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759538&dopt=Abstract
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Sequential administration of cisplatin-etoposide followed by topotecan in patients with extensive stage small cell lung cancer. A multicenter phase II study. Author(s): Mavroudis D, Pavlakou G, Blazoyiannakis G, Veslemes M, Apostolopoulou F, Kouroussis Ch, Kakolyris S, Agelaki S, Androulakis N, Vardakis N, Magkanas E, Samonis G, Georgoulias V. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 71-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499097&dopt=Abstract
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Sequential high-dose chemotherapy with autologous stem cell support in patients with limited-stage small cell lung cancer. Author(s): Ziske C, Gorschluter M, Mey U, Offergeld R, Glasmacher A, Schmidt-Wolf IG. Source: Anticancer Res. 2002 November-December; 22(6B): 3723-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552983&dopt=Abstract
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Staging of non-small-cell lung cancer and application of FDG-PET. A cost modeling approach. Author(s): Verboom P, Herder GJ, Hoekstra OS, Smit EF, van den Bergh JH, van Velthoven PC, Grijseels EW.
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Source: International Journal of Technology Assessment in Health Care. 2002 Summer; 18(3): 576-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391950&dopt=Abstract ·
Staging tools for nonsmall cell lung cancer. Author(s): Zawin M. Source: Respir Care Clin N Am. 2003 March; 9(1): 77-118, Vi. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820713&dopt=Abstract
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Supportive care in patients with advanced non-small-cell lung cancer. Author(s): Di Maio M, Perrone F, Gallo C, Iaffaioli RV, Manzione L, Piantedosi FV, Cigolari S, Illiano A, Barbera S, Robbiati SF, Piazza E, Ianniello GP, Frontini L, Veltri E, Castiglione F, Rosetti F, De Maio E, Maione P, Gridelli C, Rossi A, Barletta E, Barzelloni ML, Signoriello G, Bilancia D, Dinota A, Rosati G, Germano D, Lamberti A, Pontillo V, Brancacio L, Crispino C, Esposito M, Battiloro C, Tufano G, Cioffi A, Guardasole V, Angelini V, Guidetti G, Barbera S, Renda F, Romano F, Volpintesta A, Robbiati SF, Sannicolo M, Filipazzi V, Esani G, Gambaro A, Ferrario S, Tinessa V, Caprio MG, Zonato S, Cabiddu M, Raina A, Veltri E, D'Aprile M, Pistillucci G, Porcile G, Ostellino O, Vinante O, Azzarello G, Gebbia V, Borsellino N, Testa A, Gasparini G, Morabito A, Gattuso D, Romito S, Carrozza F, Fava S, Calcagno A, Grimi E, Bertetto O, Ciuffreda L, Parello G, Maiorino L, Santoro A, Santoro M, Failla G, Aiello RA, Bearz A, Sorio R, Scalone S, Clerici M, Bollina R, Belloni P, Sacco C, Sibau A, Adamo V, Altavilla G, Scimone A, Spatafora M, Bellia V, Hopps MR, Monfardini S, Favaretto A, Stefani M, Corradini GM, Pavia G, Scagliotti G, Novello S, Selvaggi G, Tonato M, Darwish S, Michetti G, Belometti MO, Labianca R, Quadri A, De Marinis F, Migliorino MR, Martelli O, Colucci G, Galetta D, Giotta F, Isa L, Candido P, Rossi N, Calandriello A, Ferrau F, Malaponte E, Barni S, Cazzaniga M, Gebbia N, Valerio MR, Belli M, Colantuoni G, Capuano MA, Angiolillo M, Sollitto F, Ardizzoia A, Luporini G, Locatelli MC, Pari F, Aitini E, Pedicini T, Febbraro A, Zollo C, Di Costanzo F, Bartolucci R, Gasperoni S, Gaion F, Palazzolo G, Galligioni E, Caffo O, Cortesi E, D'Auria G, Curcio C, Vasta M, Bumma C, Celano A, Bretti S, Nettis G, Anselmo A, Mattioli R, Nistico C, Aschelter A, Foa P. Source: British Journal of Cancer. 2003 September 15; 89(6): 1013-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966418&dopt=Abstract
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Taxanes for advanced non-small cell lung cancer. Author(s): Ramalingam S, Belani CP. Source: Expert Opinion on Pharmacotherapy. 2002 December; 3(12): 1693-709. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472367&dopt=Abstract
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Taxanes in the treatment of advanced (stage III and IV) non-small cell lung cancer (NSCLC): recent developments. Author(s): Simon GR, Bunn PA Jr. Source: Cancer Investigation. 2003; 21(1): 87-104. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643013&dopt=Abstract
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The anthelmintic drug mebendazole induces mitotic arrest and apoptosis by depolymerizing tubulin in non-small cell lung cancer cells. Author(s): Sasaki J, Ramesh R, Chada S, Gomyo Y, Roth JA, Mukhopadhyay T. Source: Molecular Cancer Therapeutics. 2002 November; 1(13): 1201-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12479701&dopt=Abstract
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The clinical usefulness of post-treatment FDG-PET for prediction of prognosis in lung cancer patients treated with radiation therapy. Author(s): Nakayama Y, Kitamoto Y, Ishikawa H, Saitoh J, Sakurai H, Akimoto T, Hasegawa M, Nakano T. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2 Suppl): S410-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965801&dopt=Abstract
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The global role of irinotecan in the treatment of lung cancer: 2003 update. Author(s): Langer CJ. Source: Oncology (Huntingt). 2003 July; 17(7 Suppl 7): 30-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886872&dopt=Abstract
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The outcome of combined-modality therapy for stage III non-small-cell lung cancer in the elderly. Author(s): Schild SE, Stella PJ, Geyer SM, Bonner JA, McGinnis WL, Mailliard JA, Brindle J, Jatoi A, Jett JR; North Central Cancer Treatment Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 1; 21(17): 3201-6. Epub 2003 July 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874270&dopt=Abstract
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The protective effect of the Mediterranean diet on lung cancer. Author(s): Fortes C, Forastiere F, Farchi S, Mallone S, Trequattrinni T, Anatra F, Schmid G, Perucci CA. Source: Nutrition and Cancer. 2003; 46(1): 30-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925301&dopt=Abstract
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The role of carotenoids on the risk of lung cancer. Author(s): Epstein KR. Source: Seminars in Oncology. 2003 February; 30(1): 86-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635093&dopt=Abstract
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The role of RAD51 in etoposide (VP16) resistance in small cell lung cancer. Author(s): Hansen LT, Lundin C, Spang-Thomsen M, Petersen LN, Helleday T.
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Source: International Journal of Cancer. Journal International Du Cancer. 2003 July 1; 105(4): 472-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712436&dopt=Abstract ·
The therapeutic effects of the radiotherapy plus TCM treatment observed in senile non-parvicellular lung cancer patients at the late stage. Author(s): Lan X, Jiang Y. Source: J Tradit Chin Med. 2003 March; 23(1): 32-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747193&dopt=Abstract
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The value of [18F]fluoro-2-deoxy-D-glucose positron emission tomography in the selection of patients with stage IIIA-N2 non-small cell lung cancer for combined modality treatment. Author(s): Hoekstra CJ, Stroobants SG, Hoekstra OS, Vansteenkiste J, Biesma B, Schramel FJ, van Zandwijk N, van Tinteren H, Smit EF. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 151-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581567&dopt=Abstract
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Thermoradiotherapy for local control of chest wall invasion in patients with advanced non-small cell lung cancer. Author(s): Sakao S, Takiguchi Y, Nemoto K, Tatsumi K, Tanabe N, Kurosu K, Ooiwa T, Shirasawa H, Kuriyama T. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2002 December; 7(6): 343-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12494249&dopt=Abstract
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Three-week schedule of irinotecan and cisplatin in advanced non-small cell lung cancer: a multicentre phase II study. Author(s): Cardenal F, Domine M, Massuti B, Carrato A, Felip E, Garrido P, Juan O, Artal A, Barneto I, Lopez-Vivanco G, Balcells M, Rosell R. Source: Lung Cancer (Amsterdam, Netherlands). 2003 February; 39(2): 201-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581574&dopt=Abstract
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Tissue diagnosis of suspected lung cancer: selecting between bronchoscopy, transthoracic needle aspiration, and resectional biopsy. Author(s): Yung RC. Source: Respir Care Clin N Am. 2003 March; 9(1): 51-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820712&dopt=Abstract
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Topoisomerase inhibitor-induced apoptosis accompanied by down-regulation of Bcl2 in human lung cancer cells. Author(s): Oizumi S, Isobe H, Ogura S, Ishida T, Yamazaki K, Nishimura M, Kawakami Y, Dosaka-Akita H.
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Source: Anticancer Res. 2002 November-December; 22(6C): 4029-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553028&dopt=Abstract ·
Traditional Chinese medicine Astragalus reverses predominance of Th2 cytokines and their up-stream transcript factors in lung cancer patients. Author(s): Wei H, Sun R, Xiao W, Feng J, Zhen C, Xu X, Tian Z. Source: Oncol Rep. 2003 September-October; 10(5): 1507-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12883732&dopt=Abstract
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Transcripts in pretreatment biopsies from a three-arm randomized trial in metastatic non-small-cell lung cancer. Author(s): Rosell R, Scagliotti G, Danenberg KD, Lord RV, Bepler G, Novello S, Cooc J, Crino L, Sanchez JJ, Taron M, Boni C, De Marinis F, Tonato M, Marangolo M, Gozzelino F, Di Costanzo F, Rinaldi M, Salonga D, Stephens C. Source: Oncogene. 2003 June 5; 22(23): 3548-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12789263&dopt=Abstract
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Triplet chemotherapy with vinorelbine, gemcitabine, and cisplatin for advanced nonsmall cell lung cancer: a phase II study. Author(s): Niho S, Kubota K, Goto K, Ohmatsu H, Matsumoto T, Kakinuma R, Nishiwaki Y. Source: British Journal of Cancer. 2002 December 2; 87(12): 1360-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454762&dopt=Abstract
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Use of temozolomide with other cytotoxic chemotherapy in the treatment of patients with recurrent brain metastases from lung cancer. Author(s): Ebert BL, Niemierko E, Shaffer K, Salgia R. Source: The Oncologist. 2003; 8(1): 69-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604733&dopt=Abstract
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Usefulness of chest single photon emission computed tomography with technetium99m methoxyisobutylisonitrile to predict taxol based chemotherapy response in advanced non-small cell lung cancer. Author(s): Shih CM, Hsu WH, Huang WT, Wang JJ, Ho ST, Kao A. Source: Cancer Letters. 2003 September 10; 199(1): 99-105. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963129&dopt=Abstract
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Using technetium-99m tetrofosmin chest imaging to predict taxol-based chemotherapy response in non-small cell lung cancer but not related to lung resistance protein expression. Author(s): Shih CM, Shiau YC, Wang JJ, Ho ST, Kao A.
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Source: Lung. 2003; 181(2): 103-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953149&dopt=Abstract ·
Value of accelerated multimodality therapy in stage IIIA and IIIB non-small cell lung cancer. Author(s): DeCamp MM, Rice TW, Adelstein DJ, Chidel MA, Rybicki LA, Murthy SC, Blackstone EH. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 July; 126(1): 17-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878935&dopt=Abstract
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Value of FDG-PET in the management of non-small cell lung cancer. Author(s): Stroobants S, Verschakelen J, Vansteenkiste J. Source: European Journal of Radiology. 2003 January; 45(1): 49-59. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499064&dopt=Abstract
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Value of whole-body FDG PET in management of lung cancer. Author(s): Higashi K, Matsunari I, Ueda Y, Ikeda R, Guo J, Oguchi M, Tonami H, Yamamoto I. Source: Ann Nucl Med. 2003 February; 17(1): 1-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691125&dopt=Abstract
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Vinorelbine and carboplatin in inoperable non-small cell lung cancer: a monoinstitutional phase II study. Author(s): Cremonesi M, Mandala M, Cazzaniga M, Rezzani C, Gambera M, Barni S. Source: Oncology. 2003; 64(2): 97-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566905&dopt=Abstract
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Vinorelbine: a review of its use in elderly patients with advanced non-small cell lung cancer. Author(s): Curran MP, Plosker GL. Source: Drugs & Aging. 2002; 19(9): 695-721. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381238&dopt=Abstract
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Weekly low-dose docetaxel in advanced non-small cell lung cancer previously treated with two chemotherapy regimens. Author(s): Petrioli R, Pozzessere D, Messinese S, Sabatino M, Ceciarini F, Marsili S, Correale P, Fiaschi AI, Voltolini L, Gotti G, Francini G. Source: Lung Cancer (Amsterdam, Netherlands). 2003 January; 39(1): 85-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499099&dopt=Abstract
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Weekly paclitaxel for advanced non-small cell lung cancer patients not suitable for platinum-based therapy.
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Author(s): Juan O, Albert A, Villarroya T, Sanchez R, Casan R, Caranana V, Campos JM, Alberola V. Source: Neoplasma. 2003; 50(3): 204-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937854&dopt=Abstract ·
Weekly paclitaxel in the treatment of metastatic and/or recurrent non-small cell lung cancer. Author(s): Alberola V, Cortesi E, Juan O. Source: Critical Reviews in Oncology/Hematology. 2002 December 27; 44 Suppl: S31-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505597&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: ·
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.comÒ: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDÒHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to lung cancer; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: ·
General Overview Atherosclerosis and Heart Disease Prevention Source: Prima Communications, Inc.www.personalhealthzone.com
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Breast Cancer Source: Healthnotes, Inc.; www.healthnotes.com Breast Cancer Source: Integrative Medicine Communications; www.drkoop.com Cancer Prevention (reducing the Risk) Source: Prima Communications, Inc.www.personalhealthzone.com Cancer Prevention and Diet Source: Healthnotes, Inc.; www.healthnotes.com Chronic Obstructive Pulmonary Disease Source: Integrative Medicine Communications; www.drkoop.com Colon Cancer Source: Healthnotes, Inc.; www.healthnotes.com Emphysema Source: Integrative Medicine Communications; www.drkoop.com Lung Cancer Source: Healthnotes, Inc.; www.healthnotes.com Lung Cancer Source: Integrative Medicine Communications; www.drkoop.com Prostate Cancer Source: Healthnotes, Inc.; www.healthnotes.com Stroke Source: Healthnotes, Inc.; www.healthnotes.com ·
Alternative Therapy Nutrition Source: Integrative Medicine Communications; www.drkoop.com Reflexology Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,730,00.html
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Herbs and Supplements Asian Ginseng Source: Healthnotes, Inc.; www.healthnotes.com Astragalus Mem Alternative names: Huang-Qi; Astragalus membranaceus Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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B-carotene Source: Integrative Medicine Communications; www.drkoop.com Beta-carotene Source: Healthnotes, Inc.; www.healthnotes.com Beta-carotene Alternative names: b-carotene, Trans-beta Carotene; Provitamin A, Betacarotenum Source: Integrative Medicine Communications; www.drkoop.com Beta-carotene Source: Prima Communications, Inc.www.personalhealthzone.com Beta-carotene Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10103,00.html Betacarotenum Source: Integrative Medicine Communications; www.drkoop.com Camellia Sinensis Source: Integrative Medicine Communications; www.drkoop.com Carotenoids Source: Healthnotes, Inc.; www.healthnotes.com Carotenoids Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,763,00.html Chemotherapy Source: Healthnotes, Inc.; www.healthnotes.com Coenzyme Q10 Source: Healthnotes, Inc.; www.healthnotes.com Cyclophosphamide Source: Healthnotes, Inc.; www.healthnotes.com Docetaxel Source: Healthnotes, Inc.; www.healthnotes.com Flavonoids Source: Healthnotes, Inc.; www.healthnotes.com Fluorouracil Source: Healthnotes, Inc.; www.healthnotes.com
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Ginseng Source: Prima Communications, Inc.www.personalhealthzone.com Green Tea Alternative names: Camellia sinensis Source: Healthnotes, Inc.; www.healthnotes.com Green Tea Alternative names: Camellia sinensis Source: Integrative Medicine Communications; www.drkoop.com Melatonin Source: Healthnotes, Inc.; www.healthnotes.com Melatonin Source: Integrative Medicine Communications; www.drkoop.com Melatonin Source: Prima Communications, Inc.www.personalhealthzone.com Methotrexate Source: Healthnotes, Inc.; www.healthnotes.com Paclitaxel Source: Healthnotes, Inc.; www.healthnotes.com Panax Alternative names: Ginseng; Panax ginseng Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Thuja Plicata Alternative names: Western Red Cedar Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Trans-beta-carotene Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON LUNG CANCER Overview In this chapter, we will give you a bibliography on recent dissertations relating to lung cancer. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “lung cancer” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on lung cancer, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Lung Cancer ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to lung cancer. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: ·
4hpr-x Radiation Mechanisms of Interactions in Non-small Cell Lung Cancer (nsclc) Cells in Vitro by Nasca, Melita Maria; Phd from The Univ. of Texas H.s.c. at Houston Grad. Sch. of Biomed. Sci., 2002, 122 pages http://wwwlib.umi.com/dissertations/fullcit/3046065
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An Epidemiological Investigation of the Roles of Dietary Antioxidant Nutrients, Fruits and Vegetables, and Residential Radon Exposure in the Etiology of Lung Cancer by Wright, Margaret Elaine; Phd from Yale University, 2003, 106 pages http://wwwlib.umi.com/dissertations/fullcit/3084386
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Bcl-2 Proteins in Human Lung Cancer: Molecular Heterogeneity and Prognostic Value by Huang, Chris Ing-yi; Phd from Harvard University, 2002, 121 pages http://wwwlib.umi.com/dissertations/fullcit/3051190
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Effect of Cigarette Tar Yield and Mentholation on the Occurrence of Lung Cancer by Brooks, Daniel Rinzberg; Scd from Boston University, 2002, 126 pages http://wwwlib.umi.com/dissertations/fullcit/3043278
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Gelsolin Expression and Non-small Cell Lung Cancer by Yang, Jun; , Phd from State University of New York at Buffalo, 2002, 223 pages http://wwwlib.umi.com/dissertations/fullcit/3052559
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Gene Expression Analysis of Human Non-small Cell Lung Cancer Subtypes, Adenocarcinoma and Squamous Cell Carcinoma, and Mouse Lung Epithelial Cell Lines: Implications in Lung Tumorigenesis by Silvers, Amy Lynn; Phd from Medical College of Ohio at Toledo, 2002, 270 pages http://wwwlib.umi.com/dissertations/fullcit/3062769
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Geographic Concentrations of Lung Cancer Mortality in Texas and Their Relationships to Environmental and Socioeconomic Conditions by Zhou, Xinnong; Phd from Texas State University - San Marcos, 2000, 121 pages http://wwwlib.umi.com/dissertations/fullcit/3025226
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Investigation of the Mechanisms Responsible for Decreased Cyclin D2 in Non-smallcell Lung Cancer Cell Lines by Wu, Ding; Msbs from Medical College of Ohio at Toledo, 2002, 67 pages http://wwwlib.umi.com/dissertations/fullcit/1407774
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Isolation and Characterization of Organ Specific Neoantigen from the Urine of Lung Cancer Patients by Fink, Aaron; Phd from Mcgill University (canada), 1982 http://wwwlib.umi.com/dissertations/fullcit/NK60944
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Lung Cancer, Radon Daughter Exposure, and Smoking a Nested Case-control Study Within a Cohort of Uranium Mine Workers by L'abbé Kristan A; Phd from University of Toronto (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL46389
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Lung Cancer: Epidemiological and Clinical Studies with Special Reference to Surgical Treatment (sweden) by Myrdal, Gunnar; Phd from Uppsala Universitet (sweden), 2003, 90 pages http://wwwlib.umi.com/dissertations/fullcit/f148657
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Perceived Control As a Determinant of Preventive Action for Heart Disease and Lung Cancer by Allison, Kenneth R; Phd from University of Toronto (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL39646
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Radiosensitivity in Lung Cancer with Focus Onp53 by Bergqvist, Michael; Phd from Uppsala Universitet (sweden), 2002, 59 pages http://wwwlib.umi.com/dissertations/fullcit/f738897
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Regulation of Lung Cancer Cell Growth and Differentiation by Notch Signaling by Sriuranpong, Virote; Phd from The Johns Hopkins University, 2002, 119 pages http://wwwlib.umi.com/dissertations/fullcit/3028334
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Reliability and Validity of Proxy Reported Information in a Case-control Study of Lung Cancer by Pron, Gaylene E; Phd from University of Toronto (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL39766
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Restriction Landmark Genomic Scanning to Identify Novel Methylated and Amplified Dna Sequences in Human Lung Cancer by Dai, Zunyan; Phd from The Ohio State University, 2002, 167 pages http://wwwlib.umi.com/dissertations/fullcit/3081908
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The Chemoprevention of Lung Cancer Using Nonsteroidal Anti-inflammatory Drugs (nsaids) by Elliott, Christopher S.; Phd from The Ohio State University, 2003, 127 pages http://wwwlib.umi.com/dissertations/fullcit/3088847
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The Incidence of Lung Cancer among Schizophrenic Males Versus Nonschizophrenic Males by Breen, Mary Julie, Edd from United States International University, 1981, 100 pages http://wwwlib.umi.com/dissertations/fullcit/8117016
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The Longitudinal Effects of Cancer Treatment on Sexuality in Individuals with Lung Cancer by Shell, Judith Ann; Phd from Michigan State University, 2002, 110 pages http://wwwlib.umi.com/dissertations/fullcit/3064308
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The Relationship of Information Preferences, Family Functioning, Learned Resourcefulness, and Quality of Life among Patients with Lung Cancer by Hinds, Cora; Edd from University of Toronto (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL46318
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND LUNG CANCER Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning lung cancer.
Recent Trials on Lung Cancer The following is a list of recent trials dedicated to lung cancer.8 Further information on a trial is available at the Web site indicated. ·
Carboplatin and Etoposide With or Without Thalidomide in Treating Patients With Limited-Stage or Extensive-Stage Small Cell Lung Cancer Condition(s): extensive stage small cell lung cancer; limited stage small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): London Lung Cancer Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy such as carboplatin and etoposide use different ways to stop tumor cells from dividing so they stop growing or die. Thalidomide may stop the growth of cancer by stopping blood flow to the tumor. It is not yet known if combination chemotherapy is more effective with or without thalidomide in treating small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of combining carboplatin and etoposide with or without thalidomide in treating patients who have limited- or extensive-stage small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061919
8
These are listed at www.ClinicalTrials.gov.
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Carboplatin, Paclitaxel, and Radiation Therapy With or Without Thalidomide in Treating Patients With Stage III Non-small Cell Lung Cancer Condition(s): adenocarcinoma of the lung; adenosquamous cell lung cancer; bronchoalveolar cell lung cancer; large cell lung cancer; Non-small cell lung cancer; squamous cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Eastern Cooperative Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Thalidomide may stop the growth of non-small cell lung cancer by stopping blood flow to the tumor. It is not yet known if combination chemotherapy plus radiation therapy is more effective with or without thalidomide. PURPOSE: Randomized phase III trial to compare the effectiveness of carboplatin, paclitaxel, and radiation therapy with or without thalidomide in treating patients who have newly diagnosed stage III non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004859
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Combination Chemotherapy in Treating Patients With Stage IIIB, Stage IV, or Recurrent Non-Small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Roswell Park Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy such as gemcitabine, carboplatin, and paclitaxel use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. It is not yet known which chemotherapy regimen is more effective in treating non-small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of different combination chemotherapy regimens in treating patients who have stage IIIB, stage IV, or recurrent non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00054392
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Combination Chemotherapy Plus Thalidomide in Treating Patients With Stage IIIB or Stage IV Non-Small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Comprehensive Cancer Center of Wake Forest University; National Cancer Institute (NCI)
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Purpose - Excerpt: RATIONALE: Thalidomide may stop the growth of cancer by stopping blood flow to the tumor. Combining thalidomide with chemotherapy may kill more tumor cells and be an effective treatment for stage IIIB or stage IV non-small cell lung cancer. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy plus thalidomide in treating patients who have stage IIIB or stage IV nonsmall cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00025285 ·
Gefitinib in Treating Patients With Non-Small Cell Lung Cancer That Has Been Surgically Removed Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute of Canada; National Cancer Institute (NCI); Eastern Cooperative Oncology Group; Southwest Oncology Group Purpose - Excerpt: RATIONALE: Biological therapies such as gefitinib may interfere with the growth of the tumor cells and slow the growth of the tumor. It is not yet known if gefitinib is effective in delaying the recurrence of non-small cell lung cancer. PURPOSE: Randomized phase III trial to study the effectiveness of gefitinib in treating patients who have undergone surgery for stage IB, stage II, or stage IIIA non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049543
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Inhaled Doxorubicin in Treating Patients With Primary Lung Cancer or Lung Metastases Condition(s): lung metastases; Non-small cell lung cancer; Small Cell Lung Cancer Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of inhaled doxorubicin in treating patients who have primary lung cancer or lung metastases. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004930
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Isotretinoin With or Without Vitamin E for Prevention of Lung Cancer Condition(s): Non-small cell lung cancer; Small Cell Lung Cancer; Drug Toxicity Study Status: This study is currently recruiting patients. Sponsor(s): University of Colorado Cancer Center Purpose - Excerpt: RATIONALE: Isotretinoin may prevent the development of cancer cells. PURPOSE: Randomized double-blinded phase II trial to study the effectiveness of isotretinoin with or without vitamin E for chemoprevention of cancer in persons at high risk of developing lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002586
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Monoclonal Antibody Therapy in Treating Patients With Ovarian Epithelial Cancer, Melanoma, Acute Myeloid Leukemia, Myelodysplastic Syndrome, or Non-Small Cell Lung Cancer Condition(s): acute leukemia; atypical chronic myeloid leukemia; Melanoma; myelodysplastic and myeloproliferative disease; Non-small cell lung cancer; ovarian epithelial cancer Study Status: This study is currently recruiting patients. Sponsor(s): Dana-Farber/Harvard Cancer Center at Dana Farber Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. PURPOSE: Phase I trial to study the effectiveness of monoclonal antibody therapy in treating patients who have ovarian epithelial cancer, melanoma, acute myeloid leukemia, myelodysplastic syndrome, or non-small cell lung cancer. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00039091
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Radiation Therapy Combined With Paclitaxel and Carboplatin in Treating Patients With Stage I, Stage II, or Stage III Non-Small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Radiation Therapy Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug and giving them with specialized radiation therapy may kill more tumor cells. PURPOSE: Phase I/II trial to study the effectiveness of radiation therapy combined with paclitaxel and carboplatin in treating patients who have stage I, stage II, or stage III non-small cell lung cancer. Phase(s): Phase I; Phase II
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023673 ·
Radiation Therapy in Patients With Limited-Stage Small Cell Lung Cancer in Complete Remission Condition(s): limited stage small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Institut Gustave Roussy; EORTC Radiotherapy Cooperative Group; EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Radiation therapy uses high-energy x-rays to kill tumor cells and prevent the spread of cancer to the brain. It is not yet known if standard-dose radiation therapy is more effective than high-dose radiation therapy in preventing the spread of limited-stage small cell lung cancer cells to the brain. PURPOSE: Randomized phase III trial to compare the effectiveness of two regimens of radiation therapy in treating patients who have limited-stage small cell lung cancer in complete remission. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005062
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Radiation Therapy to Prevent Brain Metastases in Patients With Previously Treated Extensive-Stage Small Cell Lung Cancer Condition(s): extensive stage small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Cooperative Group
Radiotherapy
Cooperative
Group;
EORTC
Lung
Cancer
Purpose - Excerpt: RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. Radiation therapy to the brain may be effective in preventing brain metastases. It is not yet known if radiation therapy is effective following chemotherapy in preventing brain metastases. PURPOSE: Randomized phase III trial to determine the effectiveness of radiation therapy in preventing brain metastases in patients who have received chemotherapy for extensive-stage small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00016211 ·
TLK286 and Docetaxel in Treating Patients With Stage IIIB or Stage IV PlatinumResistant Non-Small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients.
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Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy, such as TLK286 and docetaxel, use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase I/II trial to study the effectiveness of combining TLK286 with docetaxel in treating patients who have stage IIIB or stage IV non-small cell lung cancer that is resistant to platinum chemotherapy (such as carboplatin or cisplatin). Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00068705 ·
ZD6474 and Docetaxel in Treating Patients With Locally Advanced or Metastatic NonSmall Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is currently recruiting patients. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. ZD6474 may stop the growth of tumor cells by blocking the enzymes necessary for tumor cell growth. PURPOSE: Randomized phase II trial to compare the effectiveness of different regimens of ZD6474 combined with docetaxel in treating patients who have locally advanced or metastatic non-small cell lung cancer that is refractory to platinum-based chemotherapy. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00054093
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Zileuton in Preventing Lung Cancer in Patients With Bronchial Dysplasia Condition(s): Hypopharyngeal Cancer; Laryngeal Cancer; lip and oral cavity cancer; Lung Cancer; Nasopharyngeal Cancer; Oropharyngeal Cancer Study Status: This study is currently recruiting patients. Sponsor(s): Barbara Ann Karmanos Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Chemoprevention therapy is the use of certain drugs to try to prevent the development or recurrence of cancer. The use of zileuton may be an effective way to prevent lung cancer in patients who have bronchial dysplasia. PURPOSE: Randomized phase II trial to study the effectiveness of zileuton in preventing lung cancer in patients who have bronchial dysplasia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056004
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Chemotherapy and Radiation Therapy With or Without Epoetin alfa in Treating Patients With Stage IIIA or Stage IIIB Non-Small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer; squamous cell lung cancer; bronchoalveolar cell lung cancer; stage IIIB non-small cell lung cancer; adenocarcinoma of the lung; large cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Comprehensive Cancer Center of Wake Forest University Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Epoetin alfa may stimulate red blood cell production and prevent or treat anemia in patients who are undergoing radiation therapy and chemotherapy. It is not yet known if chemotherapy combined with radiation therapy is more effective with or without epoetin alfa in treating non-small cell lung cancer. PURPOSE: Randomized phase III trial to determine the effectiveness of chemotherapy combined with radiation therapy with or without epoetin alfa in treating patients who have stage IIIA or stage IIIB non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00028938
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Chemotherapy Followed by Surgery or Radiation Therapy in Treating Patients With Stage III Non-small Cell Lung Cancer Condition(s): squamous cell lung cancer; large cell lung cancer; stage IIIA non-small cell lung cancer; adenocarcinoma of the lung; adenosquamous cell lung cancer; bronchoalveolar cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Giving a chemotherapy drug before surgery may shrink the tumor so that it can be removed during surgery. Radiation therapy uses high-energy x-rays to damage tumor cells. It is not yet known whether chemotherapy followed by surgery with or without radiation therapy is more effective than chemotherapy followed by radiation therapy alone in treating non-small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of chemotherapy followed by surgery with or without radiation therapy to that of chemotherapy followed by radiation therapy alone in treating patients who have stage III non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002623
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Chemotherapy Plus Radiation Therapy in Treating Patients With Stage I, Stage II, or Stage III Non-small Cell Lung Cancer That Cannot Be Surgically Removed Condition(s): stage I non-small cell lung cancer; stage II non-small cell lung cancer; stage III non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy used high-energy x-rays to damage tumor cells. It is not yet know whether chemotherapy followed by radiation therapy is more effective than chemotherapy given with radiation therapy for non-small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of two different regimens of chemotherapy and radiation therapy in treating patients who have unresectable stage I, stage II, or stage III non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003803
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Chemotherapy, Radiation Therapy, and Surgery in Treating Patients With Stage IIIA Non-small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Arthur G. James Cancer Hospital & Richard J. Solove Research Institute Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Drugs such as gadolinium texaphyrin may make the tumor cells more sensitive to radiation therapy. Combining chemotherapy, radiation therapy, and surgery may kill more tumor cells. PURPOSE: Phase I trial to study the effectiveness of combining carboplatin and paclitaxel, radiation therapy with gadolinium texaphyrin, and surgery in treating patients who have stage IIIA non-small cell lung cancer. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005065
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Combination Chemotherapy and Radiation Therapy in Treating Patients With Stage II or Stage III Non-small Cell Lung Cancer That Cannot Be Removed By Surgery Condition(s): stage IIIA non-small cell lung cancer; stage II non-small cell lung cancer; stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Baptist Hospital of Miami
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Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Specialized radiation therapy delivers a high dose of radiation directly to the tumor which may kill more tumor cells and cause less damage to normal tissue. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy and specialized high-dose radiation therapy in treating patients who have stage II or stage III non-small cell lung cancer that cannot be removed by surgery. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004253 ·
Combination Chemotherapy Plus Radiation Therapy Followed by Surgery in Treating Patients With Stage IIIB Non-Small Cell Lung Cancer Condition(s): stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Combining chemotherapy with radiation therapy may kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of combining chemotherapy and radiation therapy before surgery in treating patients who have stage IIIB non-small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00021112
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Combination Chemotherapy Plus Radiation Therapy in Treating Patients With Stage III Non-small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer; stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Robert H. Lurie Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Combining chemotherapy and radiation therapy may kill more tumor cells. PURPOSE: Phase I/II trial to study the effectiveness of combination chemotherapy plus radiation therapy in treating patients who have stage III non-small cell lung cancer. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004093
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Combination Chemotherapy With or Without Erlotinib in Treating Patients With Stage IIIB or Stage IV Non-Small Cell Lung Cancer Condition(s): stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Genentech Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Erlotinib may stop the growth of tumor cells by blocking the enzymes necessary for cancer growth. Combining combination chemotherapy with erlotinib may kill more tumor cells. It is not yet known if combination chemotherapy is more effective with or without erlotinib in treating nonsmall cell lung cancer. PURPOSE: Randomized double-blinded phase III trial to determine the effectiveness of combining carboplatin and paclitaxel with or without erlotinib in treating patients who have stage IIIB or stage IV non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029016
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Combination Chemotherapy With or Without Filgrastim in Treating Patients With Previously Untreated Extensive-Stage Small Cell Lung Cancer Condition(s): extensive stage small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); North Central Cancer Treatment Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. PURPOSE: Phase II trial to compare the effectiveness of combination chemotherapy with or without filgrastim in treating patients who have extensive-stage small cell lung cancer that has not been previously treated. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00028925
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Combination Chemotherapy With or Without Tirapazamine in Treating Patients With Stage IIIB or Stage IV Non-small Cell Lung Cancer Condition(s): stage IV non-small cell lung cancer; squamous cell lung cancer; stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer; adenocarcinoma of the lung; large cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Southwest Oncology Group
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Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. It is not yet known which combination chemotherapy regimen is more effective for non-small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of carboplatin plus paclitaxel with or without tirapazamine in treating patients who have stage IIIB or stage IV non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006484 ·
Comparison of Two Combination Chemotherapy Regimens in Treating Non-small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Eastern Cooperative Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. It is not yet known which combination chemotherapy regimen is more effective for treating non-small cell lung cancer. PURPOSE: Randomized phase II trial to compare the effectiveness of two combination chemotherapy regimens in treating patients who have non-small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006004
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Detection of Early Metastases in Patients With Stage I Non-small Cell Lung Cancer Condition(s): stage I non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Detecting very early metastases in bone marrow and/or lymph nodes may help doctors plan better treatment for non-small cell lung cancer. PURPOSE: Clinical trial to detect the presence of metastatic cancer in patients with stage I non-small cell lung cancer that has not been previously treated. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003006
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Docetaxel and Cisplatin in Treating Patients With Untreated Stage IIIA Non-small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer
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Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of docetaxel and cisplatin in treating patients who have untreated stage IIIA non-small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005868 ·
Docetaxel With or Without Exisulind in Treating Patients With Non-Small Cell Lung Cancer Condition(s): Non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Cell Pathways Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. It is not yet known if docetaxel is more effective with or without exisulind in treating non-small cell lung cancer. PURPOSE: Randomized phase III trial to study the effectiveness of docetaxel with or without exisulind in treating patients who have advanced non-small cell lung cancer that has not responded to previous treatment. PROTOCOL OUTLINE: This is a randomized, double-blind, placebo-controlled, multicenter study. Patients are stratified according to performance status (0 vs 1 vs 2) and extent of disease (locally advanced vs metastatic). Patients are randomized to one of two treatment arms. Arm I: Patients receive oral exisulind twice daily beginning on days -3 and continuing through day 21. Patients receive docetaxel IV over 1 hour on day 0. Arm II: Patients receive oral placebo twice daily beginning on day -3 and continuing through day 21. Patients receive docetaxel as in arm I. For subsequent courses, treatment repeats every 21 days in the absence of disease progression or unacceptable toxicity. Patients are followed every 30 days. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036322
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Donepezil and Vitamin E to Prevent Side Effects Caused By Radiation Therapy to the Head in Patients Receiving Treatment for Small Cell Lung Cancer Condition(s): extensive stage small cell lung cancer; limited stage small cell lung cancer; Depression; Delirium; Recurrent Small Cell Lung Cancer; radiation toxicity; psychosocial effects/treatment; Quality of Life Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); North Central Cancer Treatment Group
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Purpose - Excerpt: RATIONALE: Donepezil and vitamin E may be able to decrease side effects caused by radiation therapy given to prevent brain metastases in patients with small cell lung cancer. It is not yet known if donepezil and vitamin E are effective in preventing side effects caused by radiation therapy to the head. PURPOSE: Randomized phase III trial to determine the effectiveness of donepezil and vitamin E in preventing side effects caused by radiation therapy given to prevent brain metastases in patients who have small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006349 ·
Gemcitabine Plus Supportive Care in Treating Patients With Locally Advanced or Metastatic Non-Small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer; stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Christie Hospital N.H.S. Trust Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Treatment plus supportive care may improve quality of life in patients undergoing cancer treatment. PURPOSE: Randomized phase II/III trial to compare the effect of different gemcitabine regimens plus supportive care on quality of life in patients who have locally advanced or metastatic non-small cell lung cancer. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00022009
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INS316 Compared With Saline for Sputum Collection in Diagnosing Lung Cancer Condition(s): Small Cell Lung Cancer; Non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Jonsson Comprehensive Cancer Center Purpose - Excerpt: RATIONALE: INS316 may produce a better sputum sample for laboratory analysis and may provide a less invasive method of diagnosing lung cancer. PURPOSE: Randomized diagnostic trial to compare the effectiveness of INS316 with that of saline for sputum collection in diagnosing lung cancer in patients suspected of having lung cancer. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00033527
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Lometrexol Plus Folic Acid in Treating Patients With Stage IIIB or Stage IV NonSmall Cell Lung Cancer Condition(s): stage IV non-small cell lung cancer; adenosquamous cell lung cancer; squamous cell lung cancer; stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer; adenocarcinoma of the lung; large cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): Tularik Purpose - Excerpt: RATIONALE: Lometrexol may stop or slow the growth of tumor cells by blocking the enzymes necessary for tumor cell growth. Folic acid may be effective in preventing or lessening the side effects of lometrexol. Combining lometrexol with folic acid may be an effective treatment for non-small cell lung cancer. PURPOSE: Phase II trial to study the effectiveness of combining lometrexol with folic acid in treating patients who have stage IIIB or stage IV non-small cell lung cancer that has been previously treated. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00033722
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Megestrol in Treating Patients Who Are Undergoing Radiation Therapy for Lung Cancer Condition(s): limited stage small cell lung cancer; Anorexia; stage IIIA non-small cell lung cancer; stage II non-small cell lung cancer; Cachexia; stage IIIB non-small cell lung cancer; stage I non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Comprehensive Cancer Center of Wake Forest University Purpose - Excerpt: RATIONALE: Megestrol helps improve appetite. It is not yet known if megestrol is effective in limiting weight loss in patients who are undergoing radiation therapy. PURPOSE: Randomized phase III trial to determine the effectiveness of megestrol in limiting weight loss in patients who are undergoing radiation therapy for lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00031785
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Monoclonal Antibody Therapy Plus BCG in Treating Patients With Limited-Stage Small Cell Lung Cancer Condition(s): limited stage small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal
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cells. BCG may activate the immune system to kill tumor cells. Combining monoclonal antibody therapy with BCG may kill more tumor cells. It is not yet known if monoclonal antibody therapy plus BCG is an effective treatment for limited-stage small cell lung cancer. PURPOSE: Randomized phase III trial to determine the effectiveness of monoclonal antibody therapy plus BCG in treating patients who have limited-stage small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006352 ·
Nitrocamptothecin in Treating Patients With Advanced Small Cell Lung Cancer Condition(s): extensive stage small cell lung cancer; Recurrent Small Cell Lung Cancer Study Status: This study is no longer recruiting patients. Sponsor(s): European Organization for Research and Treatment of Cancer Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of nitrocamptothecin in treating patients who have advanced small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006082
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Oltipraz in the Prevention of Lung Cancer in People Who Smoke Condition(s): Small Cell Lung Cancer; prevention of lung cancer; Non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Robert H. Lurie Cancer Center Purpose - Excerpt: RATIONALE: Chemoprevention therapy is the use of certain drugs to try to prevent the development of cancer. PURPOSE: Randomized phase I trial to study the effectiveness of oltipraz in preventing lung cancer in people who smoke. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006457
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Paclitaxel and Carboplatin Chemotherapy Compared With Standard Chemotherapy in Treating Patients With Stage III or Stage IV Non-small Cell Lung Cancer That Cannot Be Removed During Surgery Condition(s): stage IIIA non-small cell lung cancer; stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients.
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Sponsor(s): Christie Hospital N.H.S. Trust Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. It is not yet known whether paclitaxel and carboplatin is more effective than standard chemotherapy for advanced non-small cell lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of paclitaxel and carboplatin chemotherapy with that of standard chemotherapy in treating patients who have stage III or stage IV non-small cell lung cancer that cannot be removed during surgery. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004887 ·
Paclitaxel and Carboplatin With or Without BMS-275291 in Treating Patients With Advanced or Metastatic Non-small Cell Lung Cancer Condition(s): stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute of Canada Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. It is not yet known whether giving paclitaxel and carboplatin with BMS-275291 is more effective than giving paclitaxel and carboplatin alone for non-small cell lung cancer. PURPOSE: Randomized phase II/III trial to compare the effectiveness of paclitaxel and carboplatin with or without BMS-275291 in treating patients who have advanced or metastatic non-small cell lung cancer. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006229
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Paclitaxel in Treating Patients With Lung Cancer Condition(s): stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer; stage IV non-small cell lung cancer; adenocarcinoma of the lung Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Lung Cancer Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of paclitaxel in treating patients who have unresectable stage IIIB, stage IV or recurrent lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002972
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Photodynamic Therapy With HPPH in Treating Patients With Early Stage Lung Cancer Condition(s): squamous cell lung cancer; stage 0 non-small cell lung cancer; adenocarcinoma of the lung; large cell lung cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Roswell Park Cancer Institute Purpose - Excerpt: RATIONALE: Photodynamic therapy uses light and drugs that make tumor cells more sensitive to light to kill tumor cells. Photosensitizing drugs such as HPPH are absorbed by tumor cells and, when exposed to light, become active and kill the tumor cells. PURPOSE: Phase I trial to study the effectiveness of photodynamic therapy with HPPH in treating patients who have early stage lung cancer. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00025571
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Topotecan and Paclitaxel in Treating Patients With Recurrent or Refractory Small Cell Lung Cancer Condition(s): Recurrent Small Cell Lung Cancer Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); North Central Cancer Treatment Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of topotecan and paclitaxel in treating patients who have recurrent or refractory small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003281
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Celecoxib and Docetaxel in Treating Patients With Advanced Non-Small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer; stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer Study Status: This study is suspended. Sponsor(s): Barbara Ann Karmanos Cancer Institute Purpose - Excerpt: RATIONALE: Celecoxib may slow the growth of cancer by stopping blood flow to the tumor. Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining chemotherapy with celecoxib may kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of combining celecoxib and docetaxel in treating patients who have advanced non-small cell lung cancer that has been previously treated with platinum -based chemotherapy. Phase(s): Phase II
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00030420 ·
Chemotherapy Plus Radiation Therapy With or Without Surgery in Treating Patients With Stage IIIA Non-small Cell Lung Cancer Condition(s): squamous cell lung cancer; adenocarcinoma of the lung; bronchoalveolar cell lung cancer; stage IIIA non-small cell lung cancer; large cell lung cancer Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Southwest Oncology Group; Eastern Cooperative Oncology Group; Cancer and Leukemia Group B; North Central Cancer Treatment Group; National Cancer Institute of Canada; Radiation Therapy Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining radiation therapy with chemotherapy may kill more tumor cells. It is not yet known if chemotherapy plus radiation therapy is more effective with or without surgery for lung cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of cisplatin and etoposide plus radiation therapy with or without surgery in treating patients with stage IIIA non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002550
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Combination Chemotherapy and Radiation Therapy in Treating Patients With Limited-Stage Small Cell Lung Cancer Condition(s): limited stage small cell lung cancer Study Status: This study is suspended. Sponsor(s): National Cancer Institute (NCI); North Central Cancer Treatment Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Combining chemotherapy with radiation therapy may kill more cancer cells. PURPOSE: Phase I/II trial to study the effectiveness of combination chemotherapy before, during, and after radiation therapy in treating patients who have limited-stage small cell lung cancer. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006012
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Combination Chemotherapy Plus Fluoxetine in Treating Patients With Advanced or Recurrent Non-Small Cell Lung Cancer Condition(s): Anxiety Disorder; Depression; Fatigue; Non-small cell lung cancer
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Study Status: This study is suspended. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one chemotherapy drug may kill more cancer cells. An antidepressant such as fluoxetine may improve the quality of life in patients undergoing chemotherapy. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy plus fluoxetine in treating patients who have advanced or recurrent non-small cell lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005850 ·
Depsipeptide to Treat Lung Cancer Condition(s): Lung cancer; Lung Neoplasm Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will evaluate the ability of Depsipeptide to shrink or stop the growth of tumors in lung cancer patients. This drug has shrunk tumors in various other kinds of cancers in laboratory and animal studies. Patients with lung cancer who wish to participate in this study will be screened with various tests to determine their eligibility. These include an electrocardiogram (EKG), blood tests, imaging tests (X-rays and scans), lung function tests, and a tumor biopsy. The biopsy-a procedure in which a small sample of tumor is removed-is done in one of two ways, depending on the location of the tumor: 1. The back of the throat is sprayed with a numbing medicine and a bronchoscope (a long flexible tube) is passed down the throat into the lungs to remove the tissue. This procedure is done in the operating room. Or, 2. The skin on the chest is numbed and a thin needle is inserted through the chest to the tumor, where a sample of tissue is taken. This procedure is done in the diagnostic radiology department. Study participants will undergo two 21-day treatment cycles of Depsipeptide. The drug will given in two four-hour infusions-on days one and seven of each cycle-through a catheter (long, thin plastic tube) placed in a vein in the arm or neck or under the collarbone. For each infusion, the patient will be admitted to the hospital for 24 hours. Biopsies will be repeated on day eight of both cycles. Blood samples will be taken several times during the treatment period to evaluate blood levels of the drug and its effects on the body. EKGs will also be done periodically to monitor the heart. Participants have a follow-up evaluation about two weeks after the end of treatment to determine the response to the drug. Tests will include scans of the chest, abdomen, pelvis and brain. Patients whose tumor has shrunk will be offered additional Depsipeptide cycles. This study may provide information that will lead to more effective treatments for lung cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005656
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Docetaxel With or Without Infliximab in Treating Weight Loss, Loss of Appetite, and Fatigue in Patients with Advanced Non-Small Cell Lung Cancer Condition(s): Anorexia; Cachexia; Fatigue; Non-small cell lung cancer; Quality of Life Study Status: This study is suspended. Sponsor(s): North Central Cancer Treatment Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Infliximab may improve cancer-related weight loss, lack of appetite, and fatigue. It is not yet known whether docetaxel is more effective with or without infliximab in preventing weight loss and fatigue in patients with advanced cancer. PURPOSE: Randomized phase III trial to determine the effectiveness of docetaxel with or without infliximab in preventing weight loss, loss of appetite, and fatigue in patients who have advanced non-small cell lung cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040885
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Phenylbutyrate Plus Azacitidine in Treating Patients With Acute Myeloid Leukemia, Myelodysplasia, Non-Hodgkin's Lymphoma, Multiple Myeloma, Non-small Cell Lung Cancer, or Prostate Cancer Condition(s): Lung Cancer; Leukemia; Lymphoma; Prostate Cancer Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Memorial Sloan-Kettering Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one chemotherapy drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of phenylbutyrate plus azacitidine in treating patients who have acute myeloid leukemia, myelodysplasia, non-Hodgkin's lymphoma, multiple myeloma, nonsmall cell lung cancer, or prostate cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006019
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Trastuzumab in Treating Patients With Stage IIIB or Stage IV Non-small Cell Lung Cancer That Overexpresses HER2 Condition(s): stage IV non-small cell lung cancer; stage IIIB non-small cell lung cancer; recurrent non-small cell lung cancer Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. PURPOSE: Phase II trial to study the effectiveness of trastuzumab in treating
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patients who have stage IIIB or stage IV non-small cell lung cancer that overexpresses HER2. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004883 ·
Vaccine Therapy and Sargramostim in Treating Patients With Non-small Cell Lung Cancer Condition(s): stage IIIA non-small cell lung cancer; stage IV non-small cell lung cancer; stage II non-small cell lung cancer; bronchoalveolar cell lung cancer; stage IIIB nonsmall cell lung cancer; adenocarcinoma of the lung; large cell lung cancer; stage I nonsmall cell lung cancer Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Memorial Sloan-Kettering Cancer Center Purpose - Excerpt: RATIONALE: Vaccines may make the body build an immune response to kill tumor cells. Colony-stimulating factors such as sargramostim may increase the number of immune cells found in bone marrow or peripheral blood. PURPOSE: Phase I trial to study the effectiveness of vaccine therapy and sargramostim in treating patients who have non-small cell lung cancer. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005630
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “lung cancer” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: ·
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON LUNG CANCER Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “lung cancer” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on lung cancer, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Lung Cancer By performing a patent search focusing on lung cancer, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on lung cancer: ·
Antisense oligonucleotides for IL-8 and IL-8 receptor Inventor(s): Pietrzkowski; Zbigniew (Santa Ana, CA), Olbina; Gordana (Huntington Beach, CA), Cieslak; Dariusz (Santa Ana, CA) Assignee(s): ICN Pharmaceuticals, Inc. (Costa Mesa, CA) Patent Number: 5,849,903 Date filed: February 5, 1997 Abstract: Oligonucleotides are provided which are effective in inhibiting the growth, metastasis and/or angiogenesis of tumors, including particularly melanoma and/or lung cancer. Methods are also provided for use of these oligonucleotides in the treatment of diseases. Excerpt(s): The field of the invention is oligonucleotide therapeutics, and more particularly the use of oligonucleotides to modulate the expression of IL-8 and/or IL-8 Receptor to control growth, metastasis and/or angiogenesis in tumors. Interleukin-8 (IL8, neutrophil activating protein-1, or NAP-1) is a member of C-X-C chemokine family of related cytokines having broad involvement in inflammatory responses, tissue injury, growth regulation and cellular adhesion. Cerretti, D. P., et al., Molecular Characterization of Receptors for Human Interleukin-8, GRO/Melanoma GrowthStimulatory Activity and Neutrophil Activating Peptide-2, Molecular Immunology, 30(4), 359-367 (1993); and Koch, A. E., et al., In situ expression of cytokines and cellular adhesion molecules in the skin of patients with systemic sclerosis, Pathobiology, 61(5-6), 239-46 (1993). A review of the C-X-C family is given in Streiker, R. M., et al., Role of C-XC Chemokines As Regulators Of Angiogenesis In Lung Cancer, J. of Leukocyte Biology, 57, 752-762 (1995). IL-8 has also been shown to have a potent stimulatory effect on angiogenesis. See, e.g., Koch, A. E., Interleukin-8 as a Macrophage-Derived Mediator of Angiogenesis, Science, 258, 1798-1800 (1992). It is known that IL-8 is produced by a variety of normal human somatic cells including monocytes/macrophages, dermal fibroblasts, vascular endothelial cells, keratinocytes, and mesangeal cells. Yasumoto, K., et al., Tumor Necrosis Factor Alpha and Interferon Gamma Synergistically Induce Interleukin 8 Production in a Human Gastric Cancer Cell Line Though Acting Concurrently on AP-1 and NF-kB-like Binding Sites of the Interleukin 8 Gene, J. of Biological Chemistry, 267(31), 22506-11 (1992). Apparently, such cells produce IL-8 only when stressed, and not under conditions of normal growth and homeostasis,. Factors which induce IL-8 production include inflammation, IL-1, TNF, LPS and thrombin. Web site: http://www.delphion.com/details?pn=US05849903__
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Breath test for detection of lung cancer Inventor(s): Phillips; Michael (1 Horizon Rd., Fort Lee, NJ 07024) Assignee(s): none reported Patent Number: 6,312,390 Date filed: October 1, 1999 Abstract: Carcinogenesis is accompanied by increased production of oxygen free radicals (OFRs) which degrade membranes by lipid peroxidation. The process evolves
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volatile organic compounds (VOCs), principally alkanes, which are excreted in the breath. VOCs in alveolar breath provided sensitive and specific markers of lung cancer. Breath VOC analysis is a non-invasive test which may potentially detect lung cancer at an early stage and reduce the high mortality of the disease. Excerpt(s): The invention relates to methods of detecting and diagnosing lung cancers in mammals. Primary carcinoma of the lung is the leading cause of cancer death in the United States. Every year, more than 100,000 males and 50,000 females develop lung cancer, and most of them die within twelve months. There is a clinical need for a screening test which can detect lung cancer in its earliest stages because prompt treatment of localized disease improves the 5-year survival rate to 30% in males and 50% in females. However, most cases are not detected until local or metastatic growth causes symptoms, and prospective screening with frequent radiography and sputum cytology has not improved the survival rate in smoking males aged 45 years or older. Since early detection of lung cancer can potentially reduce mortality, researchers have investigated alternative diagnostic technologies such as breath testing. The rationale of a breath test for lung cancer is based upon three observations: first, carcinogenesis is accompanied by increased production of oxygen free radicals (OFRs), second, OFRs degrade cell membranes by lipid peroxidation, evolving alkanes such as ethane and pentane, and third, these alkanes are volatile organic compounds (VOCs) which are excreted in the breath. Web site: http://www.delphion.com/details?pn=US06312390__ ·
Cancer treatment with Go 6976 Inventor(s): Lu; Zhimin (10172 Black Mountain Rd., Apt. 103, San Diego, CA 92126), Wang; Keming (79 East Ximei Street, Apt. 303, Suzhou, CN) Assignee(s): none reported Patent Number: 6,303,646 Date filed: August 9, 1999 Abstract: A chemotheraputic cancer treatment in which Go6976 or one of its derivatives is administered to a mammal for the treatment of the cancer. The Go6976 or its derivative is directed to PKC.alpha. activity. Experiments have shown Go6976 to be effective for the treatment of breast cancer, leukemia, lung cancer, bone cancer and skin cancer. These treatments may be accomplished utilizing Go6976 or its derivatives alone or in combination with other prior art chemotherapy agents or in combination with radiation therapy. In a preferred embodiment Go6976 is used for the treatment of cancer as a preventative drug by preventing cancer cell formation. Excerpt(s): This invention relates to cancer treatments and especially to cancer treatments directed to protein kinase C.alpha. enzyme. Researchers have recognized that a family of enzymes known as protein kinase C enzymes is associated with a large number of cancers. This family includes at least eleven isoenzymes. A particular member of this family is identified as the protein kinase C alpha enzyme, abbreviated: PKC.alpha. Researches have reported increases in PKC.alpha. activity in human breast tumors (NG et al., Science. 283:2085-2089) and significant increases in PKC.alpha. expression in prostate cancers (Cornford et al., Am. J. Pathol. 154: 137-144). Researchers have reported that PKC.alpha. is required for the metastasis of human melanoma (Dennis et al., Cancer Lett. 128:65-70) and that PKC.alpha. is related to the progression of brain tumors (Shen et al., Mol. Pharmacol. 55:396-402). There is general agreement
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among many cancer researchers that some of the most dangerous cancers can be treated with chemotheraputic agents or specially designed oligonuclotides targeted to PKC.alpha. Web site: http://www.delphion.com/details?pn=US06303646__ ·
Compounds and methods for therapy and diagnosis of lung cancer Inventor(s): Fanger; Gary R. (Mill Creek, WA), Hosken; Nancy A. (Seattle, WA), Bangur; Chaitanya S. (Seattle, WA), Wang; Tongtong (Medina, WA), Fan; Liqun (Bellevue, WA), Kalos; Michael D. (Seattle, WA) Assignee(s): Corixa Corporation (Seattle, WA) Patent Number: 6,518,256 Date filed: April 4, 2000 Abstract: Compounds and methods for the treatment and diagnosis of lung cancer are provided. The inventive compounds include polypeptides containing at least a portion of a lung tumor protein. Vaccines and pharmaceutical compositions for immunotherapy of lung cancer comprising such polypeptides, or DNA molecules encoding such polypeptides, are also provided, together with DNA molecules for preparing the inventive polypeptides. Excerpt(s): The present invention relates generally to therapy and diagnoses of cancer, such as lung cancer. The invention is more specifically related to polypeptides comprising at least a portion of a lung tumor protein, and to polynucleotides encoding such polypeptidies. Such polypeptides and polynucleotides may be used in vaccines and pharmaceutical compositions for prevention and treatment of lung cancer, and for the diagnosis and monitoring of such cancers. Lung cancer is the primary cause of cancer death among both men and women in the U.S., with an estimated 172,000 new cases being reported in 1994. The five-year survival rate among all lung cancer patients, regardless of the stage of disease at diagnosis, is only 13%. This contrasts with a fiveyear survival rate of 46% among cases detected while the disease is still localized. However, only 16% of lung cancers are discovered before the disease has spread. Early detection is difficult since clinical symptoms are often not seen until the disease has reached an advanced stage. Currently, diagnosis is aided by the use of chest x-rays, analysis of the type of cells contained in sputum and fiberoptic examination of the bronchial passages. Treatment regimens are determined by the type and stage of the cancer, and include surgery, radiation therapy and/or chemotherapy. In spite of considerable research into therapies for the disease, lung cancer remains difficult to treat. Web site: http://www.delphion.com/details?pn=US06518256__
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Control of CD44 gene expression for therapeutic use Inventor(s): Pietrzkowski; Zbigniew (Santa Ana, CA), Ruzdijic; Sabera (Santa Ana, CA), Cieslak; Dariusz (Santa Ana, CA) Assignee(s): ICN Pharmaceuticals, Inc. (Costa Mesa, CA) Patent Number: 5,990,299 Date filed: August 14, 1995
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Abstract: Neoplastic cells which over-express CD44, including especially non-small cell lung cancer and melanoma cancer cells, are treated with antisense oligonucleotides to control CD44 expression. Test results show that the claimed oligonucleotides significantly decreases cell growth in a CD44 sequence specific manner of lung cancer or melanoma cells, or both, but are largely non-toxic to normal cells. Examples of dosing in a clinical setting are provided. Excerpt(s): The present invention relates to the field of cancer therapy, and more particularly to the use of antisense oligonucleotides to control the expression of CD44. Within a single cell CD44 may be expressed as two or more variants, presumably depending on the changing needs of the cell. The polymorphic diversity of the variants is generated by alternative splicing of the CD44 mRNA, which occurs when the various coding sequences (exons) of CD44 genes are transcribed (expressed) in different combinations. Protein products of splice variants (isoforms) of CD44 vary widely in size (from 110 kDa to more than 250 kDa) and in function. The extracellular domain of CD44 protein is known to involve cell-cell adhesion and the binding of extracellular matrix components including hyaluronic acid, fibronectin and collagen, while the intracellular domain of CD44 has been associated with ankyrin cytoskeletal proteins critical for CD44-dependent cellular mobility. CD44 has also been found to function in hematopoiesis and in lymphocyte infiltration into general circulation (4, 5, 6). The various functions of CD44 are intriguing because they can be used to explain similar behaviors between activated lymphocytes and metastasizing tumor cells. Both types of cells have relatively high expression of CD44, and both show invasive behavior, cell migration involving reversible adhesive contacts, accumulation and expansion in lymphoid tissue, and release into general circulation (6). The association with lymphoid tissue is especially interesting in that both lymphocytes and metastasizing tumor cells use CD44 variants to bind a specific ligand residing either in the extracellular matrix of the lymph nodes or on the surface of dendritic or other cells of the lymphoid tissue. Moreover, following growth and differentiation in the lymph nodes, both lymphocytes and tumor cells are synchronously released into the efferent lymphatic vessels in the general circulation. The release process requires a complex series of interactions between the lymphocytes and tumor cells, the extracellular matrix component and surrounding cells, and probably involves adhesion receptors, proteolytic enzymes, growth factors and growth factor receptors. These processes may be dependent upon clipping of the CD44 molecules, and specificity in the process may be mediated by tissue-specific ligands interacting with CD44 isoforms. Expression of CD44 in malignant cells is therefore an important factor in primary tumor growth, local invasiveness and metastatic proclivity (7,8,9). The CD44 gene locus in human genome is on chromosome 11p13 (10). Recently, most of the genomic structure of the human CD44 gene has been established (11). Over a length of about 60 kilobases (kb), at least 20 exons are distributed. Ten of these encode sequences for the standard form of CD44 (exons 1-5 and 16-20). Between exons 5 and 16, at least ten further exons are localized, which are subjected to alternative splicing (exons 6-15). In humans as in other species, the CD44 gene codes a variety of alternatively spliced proteins having different sizes and functions. Several CD44 isoforms have been purified and characterized to date, including an 89-90 kDa glycoprotein referred to as the "standard" or "hematopoietic" isoform (CD44s), and 180 kDa or more glycoproteins referred to as "epithelial" or variant isoforms (CD44v). Isolation and characterization of cDNA clones encoding the standard and epithelial isoforms have shown that the protein sequences are identical except that the epithelial isoforms contain additional sequences of 134 or more amino acids arising from at least ten exons (v1-v10 ) which code for extra-cellular domain, and the epithelial isoforms are more heavily glycosylated (12, 29). While it is now recognized that the
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CD44 standard form plays a key role in the control of cell migration, the precise functions of the alternatively spliced CD44 variants, which predominate in most cell types are unknown. Web site: http://www.delphion.com/details?pn=US05990299__ ·
Cytolytic bradykinin antagonists Inventor(s): Whalley; Eric T. (Golden, CO), Gera; Lajos (Denver, CO), Chan; Daniel C. (Denver, CO), Stewart; John M. (Denver, CO) Assignee(s): University of Colorado (Boulder, CO), Cortech, Inc. (Denver, CO) Patent Number: 5,849,863 Date filed: September 8, 1995 Abstract: The present invention provides bradykinin antagonists effective to inhibit cancer cell growth. Also provided are methods of inhibiting lung cancer cell growth by administering a therapeutically effective amount of a dimerized bradykinin antagonist. Excerpt(s): Bradykinin (BK) is a potent inflammatory peptide whose generation in tissues and body fluids elicits many physiological responses including vasodilation, smooth muscle spasm, edema, as well as pain and hyperalgesia (Burch et al., "Molecular Biology and Pharmacology of Bradykinin Receptors", Landes Comp. (1993); Burch, edited: "Bradykinin Antagonists", Dekker (1991)). There is increasing evidence that BK and related kinins contribute to the inflammatory response in acute and chronic diseases including allergic reactions, arthritis, asthma, sepsis, viral rhinitis, and inflammatory bowel disease. Recently BK was implied to be involved as an autocrine in the pathogenesis of human lung cancer (Bunn et al., Proc Natl. Acad.Sci. USA 87:2162-2166 (1990); Bunn et al., Cancer Research 52:24-31 (1992)). BK has been shown to be the most potent peptide stimulant of intracellular Ca.sup.++ release in the highest fraction of human lung cancer cell lines (Bunn et al., Cancer Research 52:24-31 (1992)). The design and synthesis of specific, potent and stable bradykinin antagonists (BKA) has long been considered a desirable goal in medicinal chemistry. In the past few years, efforts have been directed towards the development of potent BK antagonists as a means for the chemoprevention and therapeutic treatment of human lung cancers. Lung cancer is the second most common and the most lethal cancer in the United States. A large fraction of lung cancers (all small cell lung cancers (SCLC), some adenocarcinomas and a few squamous carcinomas) have a neuroendocrine phenotype (Becker et al., "The Endocrine Lung in Health & Disease", Saunders (1984)). These cancers and their premalignant precursors utilize a neuropeptide autocrine/paracrine growth factor pathway, i.e., they produce a variety of neuropeptides, express cell surface receptors for these peptides, and show autocrine stimulation by these peptides. Over the years, a number of specific and potent neuropeptide antagonists (including bradykinin, bombesin, cholecystokinin and many others) and anti-peptide antibodies were developed and used in an attempt to inhibit the growth of the lung cancer cells which expressed receptors for these specific neuropeptides (Bunn et al., Cancer Research 54:3602-3610 (1994)). However, this approach failed to inhibit a majority of lung cancer cells because of the heterogeneity of neuropeptide receptor expression among the lung cancer cells. It has been shown that broad spectrum substance P derivatives inhibited the growth of several lung cancer cell lines. However, very high concentrations (>40.mu.M) of these compounds were required, presumably because this interference occurs at the downstream level of the signal pathway (Bunn et al., Cancer Research 54:3602-3610 (1994)). It is thus desirable to provide neuropeptide antagonists with improved potency and specificity.
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Web site: http://www.delphion.com/details?pn=US05849863__ ·
Detecting cancerous conditions by assaying for telomerase activity Inventor(s): West; Michael D. (Boston, MA), Kim; Nam Woo (San Jose, CA), Weinrich; Scott L. (Redwood City, CA), Wright; Woodring E. (Dallas, TX), Harley; Calvin B. (Palo Alto, CA), Shay; Jerry W. (Dallas, TX) Assignee(s): The University of Texas Systems (Austin, TX), Geron Corporation and Board of Regents (Menlo Park, CA) Patent Number: 6,391,554 Date filed: November 23, 1999 Abstract: Methods and kits are provided for diagnosis of specific cancerous conditions. The invention features a method for diagnosis of a condition in a patient associated with an elevated level of telomerase activity within a cell. The method involves determining the presence or amount of telomerase within the cells in the patient, e.g. by the use of the polymerase chain reaction. In one embodiment of the invention, the condition associated with elevated telomerase activity is chosen from prostate cancer, breast cancer, colon cancer, renal cancer, ovarian/cervical cancer, lung cancer, and leukemia. The invention allows cancer to be detected even in tissues and cells which are not positive by pathology. Excerpt(s): This invention relates to methods for diagnosis of cellular senescence and immortalization. The following is a general description of art relevant to the present invention. None is admitted to be prior art to the invention. Michael D. West et al., entitled "Therapy and Diagnosis of Conditions Related to Telomere Length and/or Telomerase Activity," U.S. application Ser. No. 08/151,477, filed Nov. 12, 1993, and PCT WO 93/04546 filed Nov. 25, 1993, both hereby incorporated by reference, generally describe art which relates to cellular senescence, and theories or hypotheses which explain such aging and the mechanisms by which cells escape senescence and immortalize. West et al. discusses the use of telomerase activity detection for diagnosis of various cancerous conditions. Web site: http://www.delphion.com/details?pn=US06391554__
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Dihalocephalomannine and methods of use therefor Inventor(s): Pandey; Ramesh C. (Highland Park, NJ), Yankov; Luben K. (Edison, NJ) Assignee(s): Xechem International, Inc. (New Brunswick, NJ) Patent Number: 5,840,748 Date filed: December 13, 1995 Abstract: Provided are antineoplastic derivatives by a process of selective halogenation of side chains of unsaturated taxanes; more particularly, the process involves the use of halogens, particularly bromine, which is easily added to the side chain double bond of cephalomannine, leaving paclitaxel unchanged, and wherein diastereomeric mixtures of 2", 3"-dibromocephalomannine display high activity against: Leukemia cell line HL-60 (TB); Non-Small Cell Lung Cancer line NCI-H522; Colon Cancer cell lines COLO 205 and HT 29; CNS Cancer cell lines SF-539 and SNB-75; Ovarian Cancer Cell line OVCAR-
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3; Renal Cancer cell line RXF-393; and Breast Cancer cell lines MCF7, MDA-MB231/ATCC, HS 578T, MDA-MB-435 and MDA-N. Excerpt(s): This invention relates to halogenated cephalomannine, especially 2", 3"dibromocephalomannine, its preparation, methods of its use as an effective antitumor agent and as an alternative to paclitaxel in bioactivity testing. Cephalomannine is a natural product which can be found in the bark of the pacific yew tree Taxus brevifolia, and such other yew species as T. baccata, T. cuspidata, as well as T. yannanensis and other plant materials including T. hicksii, T. densiformis, T. gem, T. wardii, T. cuspidata, T. capitata, T. brownii and T. dark green spreader. It can also be found in Cephalotaxus species, such as, for example, Cephalotaxus mannii as well as cultured plant cells and fungi. Cephalomannine is most often present with its well known and structurally similar analog, paclitaxel, the structures of both which are shown in FIGS. 1 and 2. Paclitaxel has been approved by the Food and Drug Administration for treatment of ovarian cancer and breast cancer. At present it is undergoing clinical trials for treatment of various other cancers. Web site: http://www.delphion.com/details?pn=US05840748__ ·
Epithelial protein and DNA thereof for use in early cancer detection Inventor(s): Tockman; Melvin S. (Baltimore, MD), Mulshine; James L. (Bethesda, MD) Assignee(s): The United States of America as represented by the Department of Health and (Washington, DC), The Johns Hopkins University (Baltimore, MD) Patent Number: 6,251,586 Date filed: October 2, 1996 Abstract: The present invention is a purified and isolated epithelial protein, peptide and variants thereof whose increased presence in an epithelial cell is indicative of precancer. One epithelial protein which is an early detection marked for lung cancer was purified from two human lung cancer cell lines, NCI-H720 and NCI-H157. Using a six-step procedure, the epithelial protein was purified using a Western blot detection system under both non-reducing and reducing conditions. Purification steps included anion exchange chromatography, preparative isoelectric focusing, polymer-based C.sub.18 HPLC and analytic C.sub.4 HPLC. After an approximately 25,000 fold purification the immunostaining protein was >90% pure as judged by coomassie blue staining after reducing SDS-PAGE. The primary epithelial protein share some sequence homology with the heterogeneous nuclear ribonucleoprotein (hnRNP) A2. A minor co-purifying epithelial protein shares some sequence homology with the splice variant hnRNP-B1. Molecular analysis of primary normal bronchial epithelial cell cultures demonstrated a low level the epithelial protein expression, consistent with immunohistochemical staining of clinical samples, and an increased level of expression in most lung cancer cells. The epithelial protein is a marker of epithelial transformation in lung, breast, bone, ovary, prostate, kidney, melanoma and myeloma and may be casual in the process of carcinogenesis. Methods are provided for monitoring the expression of the epithelial protein, peptides and variants using molecular and immunological techniques as a screen for precancer and cancer in mammals. A method of computerized diagnoses of cancer and precancer is provided which detects levels of hnRNP messenger RNA. Excerpt(s): The present invention relates to the area of cancer diagnostics and therapeutics. More specifically, the invention relates to the isolation and purification of an early cancer detection marker protein of epithelial cells and the cloning of the DNA
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sequence encoding the protein. The invention further relates to the protein and DNA sequence for detecting and diagnosing individuals predisposed to cancer. The present inventin relates to a computerized method for generating a discriminant function predictive of cancer. The present invention also relates to therapeutic intervention to, regulate the expression of the gene product. Lung cancer is the most frequent cause of cancer death of both males and females in the United States, accounting for one in three cancer deaths.sup.(1). In the last thirty years, cancer-related survival of this disease has improved only minimally. Successful treatment of this disease by surgical resection and drug chemotherapy is strongly dependent on identification of early-stage tumors. A conceptually attractive early detection approach is to establish the presence of a cancer by evaluation of shed bronchial epithelial cells. In the late 1960's Saccomanno et al. proposed the use of sputum cytology to evaluate cytomorphologic changes in the exfoliated bronchial epithelium as a technique to enhance the early detection of lung cancer.sup.(2). However, clinical trials using combination chest X-ray and sputum cytology have not shown any decrease in cancer-related mortality.sup.(3). In 1988, Tockman et al. reported a sensitive method for early lung cancer detection by immunostaining cells contained within sputum samples with two lung cancerassociated monoclonal antibodies.sup.(4). The basis for this approach was to identify early pre-neoplastic changes in cells shed from bronchial epithelium. The antibodies used in that study were mouse monoclonal IgG's designated 703D4, disclosed in U.S. Pat. No. 4,569,788, and 624H12. In an analysis of the contribution of the individual monoclonal antibodies to early detection of lung cancer, 703D4 alone identified 20 of the 21 detected true positive cases (4; U.S. Ser. No. 08/152,881 which issues to U.S. Pat. No. 5,455,159 on Oct. 3, 1995). 624H12 has been shown to detect an oncofetal antigen which is the Lewis.sup.x -related portion of a cell-surface glycoprotein (Mulshine/Magnani). The antigen for 703D4 was unknown. Web site: http://www.delphion.com/details?pn=US06251586__ ·
Gene therapy for solid tumors using adenoviral vectors comprising suicide genes and cytokine genes Inventor(s): Chen; Shu-Hsia (Houston, TX), Woo; Savio L. C. (Houston, TX) Assignee(s): Baylor College of Medicine (Houston, TX) Patent Number: 6,066,624 Date filed: February 15, 1996 Abstract: The present invention provides a novel method of treating localized solid tumors and papillomas in an individual, as well as metastatic carcinomas. The method comprises delivering a suicide gene, by way of a recombinant adenoviral vector or other DNA transport system, into the tumor, papilloma or wart of an individual. Subsequently, a prodrug, such as the drug gaciclovir.TM., is administered to the individual. Additionally, the present invention provides a method for treating solid tumors, papillomas, warts and metastatic carcinomas, said method comprising introducing both a suicide gene and one or more cytokine genes into the tumor, papilloma or wart of an individual, and subsequently administering a prodrug to the individual. The methods of the present invention may be used to treat several different types of cancers and papillomas, including colon carcinoma, prostate cancer, breast cancer, lung cancer, melanoma, hepatoma, brain lymphoma and head and neck cancer. Excerpt(s): The present invention relates generally to the field of gene therapy. More particularly, the present invention relates to a novel gene therapy method of treating
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solid tumors, papillomas and warts using an adenoviral vector, a combination of adenoviral vectors, other viral vectors, and non-viral DNA transporter systems. Direct introduction of therapeutic genes into malignant cells in vivo can provide an effective treatment of localized tumors. Several novel treatment modalities have recently been attempted. For example, one treatment involves the delivery of normal tumor suppressor genes and/or inhibitors of activated oncogenes into tumor cells. A second treatment involves the enhancement of immunogeneity of tumor cells in vivo by the introduction of cytokine genes. A third treatment involves the introduction of genes that encode enzymes capable of conferring to the tumor cells sensitivity to chemotherapeutic agents. The herpes simplex virus-thymidine kinase (HSV-TK) gene can specifically convert a nucleoside analog (ganciclovir) into a toxic intermediate and cause death in dividing cells. It has recently been reported by Culver et al. (Science 256:1550-1552, 1992) that after delivery of the HSV-TK gene by retroviral transduction, subsequent ganciclovir treatment effectively caused brain tumor regression in laboratory animals. An attractive feature of this treatment modality for localized tumors is the so called "bystander" effect. In the "by-stander" effect, the HSV-TK expressing tumor cells prevent the growth of adjacent non-transduced tumor cells in the presence of ganciclovir. Thus, not every tumor cell has to express HSV-TK for effective cancer treatment. The HSV-TK retrovirus used by Culver et al., however, was limited by low viral titer. Thus, effective treatment of brain tumors necessitated the inoculation into animals of virus-producing cells rather than the viral isolate itself. Additionally, in previous experiments with synergeneic rats treated with a retrovirus and ganciclovir, the tumors were necrotic and were invaded by macrophages and lymphocytes. In Example 1, below, athymic mice were used and the tumor cells were destoyed without apparent involvement of the cellular immune response. The prior art remains deficient in the lack of an efficient gene therapy technique for the treatment of solid tumors. Web site: http://www.delphion.com/details?pn=US06066624__ ·
Hybridomas for lung cancer marker and monoclonal antibodies thereof Inventor(s): Bollon; Arthur P. (Dallas, TX), Torczynski; Richard M. (Farmers Branch, TX) Assignee(s): Cytoclonal Pharmaceutics, Inc. (Dallas, TX) Patent Number: 6,117,981 Date filed: June 3, 1999 Abstract: Hybridomas secreting monoclonal antibodies specific for an epitope found in the amino acids of LCGA associated with non-small cell lung carcinoma protein have been found. The monoclonal antibodies produced by these hybridomas can be used in in vivo and in vitro clinical diagnosis of non-small cell lung carcinoma and ovarian carcinoma and as target selective carriers for various anti-tumor agents and radioimaging agents. Excerpt(s): Lung cancer is the most common form of cancer in the world. Typical diagnosis of lung cancer combines x-ray with sputum cytology. Unfortunately, by the time a patient seeks medical attention for their symptoms, the cancer is at such an advanced state it is usually incurable. Consequently, research has been focused on early detection of tumor markers before the cancer becomes clinically apparent and while the cancer is still localized and amenable to therapy. The World Health Organization has classified lung cancer into four major histological or morphological types: (1) squamous cell carcinoma, (2) adenocarcinoma, (3) large cell carcinoma, and (4) small cell lung carcinoma. (World Health Organization. 1982. "The World Health Organization
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Histological Typing of Lung Tumors," Am J Clin Pathol 77:123-136). However, there is a great deal of tumor heterogeneity even within the various subtypes, and it is not uncommon for lung cancer to have features of more than one morphological subtype. The term "non-small cell lung carcinoma" (NSCLS) has been used to distinguish squamous carcinomas, adenocarcinomas, and large cell carcinomas from small cell lung carcinomas. Particular interest has been given to the identification of antigens associated with lung cancer. These antigens have been used in screening, diagnosis, clinical management, and potential treatment of lung cancer. For example, carcinoembryonic antigen (CEA) has been used as a tumor marker of cancer including lung cancer. (Nutini, et al. 1990. "Serum NSE, CEA, CT, CA 15-3 levels in human lung cancer," Int J Biol Markers 5:198-202). Squamous cell carcinoma antigen (SCC) is another established serum marker. (Margolis, et al. 1994. "Serum tumor markers in non-small cell lung cancer," Cancer 73:605-609.). Other serum antigens for lung cancer include antigens recognized by monoclonal antibodies (MAb) 5E8, 5C7, and 1F10, the combination of which distinguishes between patients with lung cancer from those without. (Schepart, et al. 1988. "Monoclonal antibody-mediated detection of lung cancer antigens in serum," Am Rev Respir Dis 138:1434-8). Serum CA 125, initially described as an ovarian cancerassociated antigen, has been investigated for its use as a prognostic factor in NSCLC. (Diez, et al. 1994. "Prognostic significance of serum CA 125 antigen assay in patients with non-small cell lung cancer," Cancer 73:136876). Other tumor markers studied for utilization in multiple biomarker assays for lung cancer include carbohydrate antigen CA19-9, neuron specific enolase (NSE), tissue polypeptide antigen (TPA), alpha fetoprotein (AFP), HCG beta subunit, and LDH. (Mizushima, et al. 1990. "Clinical significance of the number of positive tumor markers in assisting the diagnosis of lung cancer with multiple tumor marker assay," Oncology 47:43-48; Lombardi, et al. 1990. "Clinical significance of a multiple biomarker assay in patients with lung cancer," Chest 97:639-644; and Buccheri, et al. 1986. "Clinical value of a multiple biomarker assay in patients with bronchogenic carcinoma," Cancer 57:2389-2396). Web site: http://www.delphion.com/details?pn=US06117981__ ·
Inhibiting the growth p53 deficient tumor cells by administering the p53 gene Inventor(s): Mukhopadhyay; Tapas (Houston, TX), Roth; Jack A. (Houston, TX), Tainsky; Michael A. (Houston, TX) Assignee(s): Board of Regents, The University of Texas System (Austin, TX) Patent Number: 6,017,524 Date filed: October 13, 1992 Abstract: Disclosed are methods and compositions for the selective manipulation of gene expression through the preparation of retroviral expression vectors for expressing antisense sequences, such as K-ras oncogene antisense sequences, or sequences encoding a desired product, such as wild type p53 sequences. Preferred retroviral vectors of the present invention incorporate the.beta.-actin promoter in a reverse orientation with respect to retroviral transcription. Preferred antisense RNA constructs of the present invention employ the use of antisense intron DNA corresponding to distinct intron regions of the gene whose expression is targeted for down-regulation. In an exemplary embodiment, a human lung cancer cell line (NCI-H460a) with a homozygous spontaneous K-ras mutation was transfected with a recombinant plasmid that synthesizes a genomic segment of K-ras in antisense orientation. Translation of the mutated K-ras mRNA was specifically inhibited, whereas expression of H-ras and N-ras
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was unchanged. A three-fold growth inhibition occurred in H460a cells when expression of the mutated ras p21 protein was down-regulated by antisense RNA and cells remained viable. The growth of H460a tumors in nu/nu mice was substantially reduced by expressed K-ras antisense RNA. Excerpt(s): The present invention relates to methods and nucleic acid vector compositions for modifying gene expressing, involving the preparation and use of improved retroviral vectors which encode antisense RNA molecules or, alternatively, transcriptionally active RNAs that encode selected proteins. The retroviral constructs of the present invention may be employed for introducing desired gene expression units into selected target cells, such as into tumor cells within individuals afflicted with cancer. It is now well established that a variety of diseases, ranging from certain cancers to various genetic defects, are caused, at least in part, by genetic abnormalities that result in either the over expression of one or more genes, or the expression of an abnormal or mutant gene or genes. For example, many forms of cancer in man are now known to be the result of, at least indirectly, the expression of "oncogenes". Oncogenes are genetically altered genes whose altered expression product somehow disrupts normal cellular function or control (Spandidos, et al., 1989). Most oncogenes studied to date have been found to be "activated" as the result of a mutation, often a point mutation, in the coding region of a normal cellular gene or of a "protooncogene", that results in amino acid substitutions in the protein expression product. This altered expression product, in turn, exhibits an abnormal biological function that somehow takes part in the neoplastic process (Travali, et al., 1990). The underlying mutations can arise by various means, such as by chemical mutagenesis or ionizing radiation. Web site: http://www.delphion.com/details?pn=US06017524__ ·
MAP-2 as a determinant of metastatic potential Inventor(s): White; Wain (Winston-Salem, NC), Setaluri; Vijayasaradhi (Winston-Salem, NC), Fang; Dong (Winston-Salem, NC) Assignee(s): Wake Forest University Health Sciences (Winston-Salem, NC) Patent Number: 6,613,534 Date filed: March 20, 2001 Abstract: The invention relates to detection of MAP-2 (microtubule associated protein-2) as a marker to determine the metastatic potential of a tumor, including tumors derived from the neural crest such as melanomas, gliomas, Schwanomas, chromocytomas and small cell lung cancer. In one aspect, the invention comprises a method for determining the metastatic potential of a tumor sample, wherein decreased levels of MAP-2 expression in a test sample relative to controls indicates that the sample has increased metastatic potential as compared to the control. In another aspect, the invention comprises a method to prevent tumor progression in metastatic melanoma by increasing levels of MAP-2 protein in cells. Excerpt(s): The invention relates to methods for the detection, diagnosis, prognosis and treatment of cancer. Specifically, the invention describes the detection of microtubule associated protein--2 (MAP-2) in tumor cells, and the use of MAP-2 as an indicator of metastatic potential. The invention also describes the use of MAP-2 to prevent nonmetastatic primary tumors from progressing to later stage disease. Publications referred to throughout the text of this document are incorporated by reference in their entireties in order to more fully describe the state of the art as known to those skilled therein as of
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the date of the invention described and claimed herein. Cancer is the second leading cause of death in the United States after heart disease (Boring et al., CA Cancer J. Clin., 43:7 (1993)). Cancer is characterized by the growth of abnormal (neoplastic) cells which develop from normal tissue. In cancer, cells acquire the ability to override normal constraints on the cell and proliferate under conditions in which normal cells would not grow. Among the most potent cancer causing agents (carcinogens) are ultraviolet and ionizing forms of radiation. Thus, cancer is a typically a disease of malfunctioning cellular genes (or unwanted viral expression) which leads to unchecked growth of tissue. It is generally accepted that multiple mutations must occur to cause cancer, and that cells must progress through several steps in the transformation from normal cells to an early-stage tumor and finally, to invasive and metastatic disease. Web site: http://www.delphion.com/details?pn=US06613534__ ·
Method and apparatus for inducing sputum samples for diagnostic evaluation Inventor(s): Van Brunt; Nicholas P. (White Bear Lake, MN), Gagne; Donald J. (St. Paul, MN) Assignee(s): Advanced Respiratory, Inc. (St. Paul, MN) Patent Number: 6,379,316 Date filed: August 31, 1999 Abstract: An apparatus for inducing sputum samples for diagnosing pulmonary disorders, especially as it relates to detection of early stages of lung cancer. The apparatus is comprised of a pneumatic chest compression vest, a pneumatic pressure generator, and a mouthpiece connected to a nebulizer. Sputum samples are induced by applying an oscillating force to the chest via the pneumatic chest compression vest and pressure generator, while simultaneously providing an aerosolized solution (such as normal or hypertonic saline) via the nebulizer while the patient is standing. The sample is subsequently evaluated to ascertain a patient's risk of or the presence of a pulmonary disorder such as lung cancer. Excerpt(s): This application is related to "Chest Compression Vest with Front Panel Bib" and "Chest Compression Vest with Connecting Belt", which were filed on the same day and also assigned to American Biosystems. The present invention relates to an apparatus and method for inducing sputum samples from a patient. In particular, the present invention relates to obtaining high quality sputum samples for diagnosing pulmonary disorders, especially lung cancer. Lung cancer has a survival rate of only 14% and is the leading cause of cancer death in the United States. The poor prognosis for lung cancer is related to both the lack of effective early detection methods, and the inability to precisely locate the diseased area of the lung to be treated. However, improved imaging techniques now allow much better tumor location capabilities, once detected, to allow specific treatment even at very early stages. Web site: http://www.delphion.com/details?pn=US06379316__
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Method and reagent for treatment of lung cancer and other malignancies caused by the deregulation of L-MYC gene expression Inventor(s): Draper; Kenneth G. (Boulder, CO), Thompson; James D. (Boulder, CO) Assignee(s): Ribozyme Pharmaceuticals, Inc. (Boulder, CO) Patent Number: 6,492,512 Date filed: August 26, 1992 Abstract: An enzymatic RNA molecule which cleaves mRNA associated with development or maintenance of lung cancer. Excerpt(s): This invention relates to methods for inhibition of growth of transformed cells, and inhibition of progression to a transformed phenotype in pre-neoplastic cells. Transformation is a cumulative process whereby normal control of cell growth and differentiation is interrupted, usually through the accumulation of mutations affecting the expression of genes that regulate cell growth and differentiation. Scanlon WO91/18625, WO91/18624, and WO91/18913 describes a ribozyme effective to cleave oncogene RNA from the H-ras gene. This ribozyme is said to inhibit H-ras expression in response to exogenous stimuli. Reddy WO92/00080 describes use of ribozymes as therapeutic agents for leukemias, such as CML by targeting specific portions of the BCRABL gene transcript. Web site: http://www.delphion.com/details?pn=US06492512__
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Method and system for re-screening nodules in radiological images using multiresolution processing, neural network, and image processing Inventor(s): Lin; Jyh-Shyan (Derwood, MD), Lure; Yuan-Ming F (Rockville, MD), Yeh; Hwa-Young M (Potomac, MD) Assignee(s): Caelum Research Corporation (Rockville, MD) Patent Number: 6,125,194 Date filed: February 4, 1998 Abstract: An automated detection method and system improve the diagnostic procedures of radiological images containing abnormalities, such as lung cancer nodules. The detection method and system use a multi-resolution approach to enable the efficient detection of nodules of different sizes, and to further enable the use of a single nodule phantom for correlation and matching in order to detect all or most nodule sizes. The detection method and system use spherical parameters to characterize the nodules, thus enabling a more accurate detection of non-conspicuous nodules. A robust pixel threshold generation technique is applied in order to increase the sensitivity of the system. In addition, the detection method and system increase the sensitivity of true nodule detection by analyzing only the negative cases, and by recommending further re-assessment only of cases determined by the detection method and system to be positive. The detection method and system use multiple classifiers including back propagation neural network, data fusion, decision based pruned neural network, and convolution neural network architecture to generate the classification score for the classification of lung nodules. Such multiple neural network architectures enable the learning of subtle characteristics of nodules to differentiate the nodules from the corresponding anatomic background. A final decision making then selects a portion of films with highly suspicious nodules for further reviewing.
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Excerpt(s): The present invention relates to methods and systems for the digital processing of radiological images, and it more specifically relates to an automated method and system for the re-screening and detection of abnormalities, such as lung nodules in radiological chest images using multi-resolution processing, digital image processing and artificial neural networks. Lung cancer is the leading type of cancer in both men and women worldwide. Early detection and treatment of localized lung cancer at a potentially curable stage can significantly increase the patients' survival rate. Studies have shown that approximately 68% of retrospectively detected lung cancers were detected by one reader and approximately 82% were detected with an additional reader as a "second-reader". A long-term lung cancer screening program conducted at the Mayo Clinic found that 90% of peripheral lung cancers were visible in small sizes in retrospect, in earlier radiographs. Among the common detection techniques, such as chest X-ray, analysis of the types of cells in sputum specimens, and fiber optic examination of bronchial passages, chest radiography remains the most effective and widely used method. Although skilled pulmonary radiologist can achieve a high degree of accuracy in diagnosis, problems remain in the detection of the lung nodules in chest radiography due to errors that cannot be corrected by current methods of training even with a high level of clinical skill and experience. Web site: http://www.delphion.com/details?pn=US06125194__ ·
Method of inhibiting cancer growth Inventor(s): McNamara; Thomas F. (Box 44, Port Jefferson, NY 11777), Simon; Sanford (71 Cedar St., Stony Brook, NY 11790), Ramamurthy; Nungavaram S. (10 Lynam Ct., Smithtown, NY 11787), Golub; Lorne M. (29 Whitney Gate, Smithtown, NY 11787), Block; Norman L. (19000 SW. 72nd Ave., Miami, FL 33156), Selzer; Marie G. (6035 Bayview Dr., Fort Lauderdale, FL 33308), Lokeshwar; Balakrishna L. (12615 SW. 112 Ct., Miami, FL 33176), Lee; Hsi-Ming (20 Allyson Pl., Setauket, NY 11733) Assignee(s): none reported Patent Number: 6,100,248 Date filed: January 15, 1998 Abstract: The invention is a method of inhibiting cancer growth, by inhibiting cellular proliferation, invasiveness, or metastasis, or by inducing cytotoxicity against cancer in mammals. The method employs 6-demethyl-6-deoxy-4-de(dimethylamino)tetracycline (CMT-3) and other functionally related chemically modified, preferably nonantibacterial, tetracycline compounds to inhibit cancer growth. The method is particularly effective to inhibit the establishment, growth, and metastasis of solid tumors, such as tumors derived from colon cancer cells, breast cancer cells, melanoma cells, prostatic carcinoma cells, or lung cancer cells. Excerpt(s): The invention relates to methods of reducing cancer growth in biological systems. More specifically, the invention relates to the inhibition of solid tumor invasiveness and metastasis in mammals. Cancer, in all of its myriad manifestations, remains a devastating scourge upon mankind. While progress in preventing and treating cancer has been made, including particular success against Hodgkin's lymphoma and certain other forms, many types of cancer remain substantially impervious to prevailing treatment protocols. Typically, cancer is treated by chemotherapy, in which highly toxic chemicals are given to the patient, or by radiotherapy, in which toxic doses of radiation are directed at the patient. While commonly effective to kill huge numbers of cancer cells, these "cytotoxic" treatments
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also kill extraordinary numbers of healthy cells, causing the patient to experience acute debilitating symptoms including nausea, diarrhea, hypersensitivity to light, hair loss, etc. The side effects of these cytotoxic compounds limits the frequency and dosage at which they can be administered. Such disabling side effects can be mitigated to some degree by using compounds that selectively target cycling cells, i.e., interfering with DNA replication or other growth processes in cells that are actively reproducing. Since cancer cells are characterized by their extraordinary ability to proliferate, such protocols preferentially kill a larger proportion of cancer cells in comparison to healthy cells, but cytotoxicity and ancillary sickness remains a problem. Other more recent developments include efforts to develop monoclonal antibodies specific for oncogenes or HLA specificities, to identify cancer cells with great precision. However, these procedures are very expensive and extremely procedurally elaborate, yet still fail to produce the desired efficacy. Indeed, such procedures have been reported to be effective in only a small subpopulation of treated patients. Web site: http://www.delphion.com/details?pn=US06100248__ ·
Methods for analyzing PRLTS DNA Inventor(s): Nakamura; Yusuke (Kanagawa, JP), Fujiwara; Yoshiyuki (Tokyo, JP) Assignee(s): Eisai Co., Ltd. (Tokyo, JP), Cancer Institute (Tokyo, JP) Patent Number: 5,935,786 Date filed: May 6, 1997 Abstract: A gene is provided which is present in the deletion region of a chromosome common in lung cancer, hepatocellular carcinoma and colorectal cancer and encodes a novel protein, a protein encoded by the gene (PRLTS protein), and a method of discriminating tumor cells. Excerpt(s): The present invention relates to PRLTS proteins, DNAs encoding the proteins and methods of discriminating tumor cells in which use is made of the DNAs. The present invention is usefully applied in the fields of medical science and pharmaceuticals. There has long been a conception that mutations in cellular proteins play an important role in carcinogenesis. The progress of genetic engineering achieved in recent years has made it possible to analyze the amplification of the DNA encoding a specified protein and gene mutations in tumor cells, thereby rapidly advancing cancer research. The analysis and identification of genes (oncogenes) encoding proteins believed as participating in the malignant alteration of cells and the abnormal proliferation of tumor cells have been promoted, so that the identification of such genes number in the tens. On the other hand, counteracting genes (tumor suppressor genes) are highlighted in recent years. Tumor suppressor genes hitherto discovered include the Rb gene capable of suppressing retinoblastoma ›Friend, S. H., et al., Proc. Natl. Acad. Sci. USA., 84, 9095 (1987)!, the p53 gene capable of suppressing colorectal cancer ›Lane, D. P., et al., Nature, 278, 261 (1979)!, the APC gene capable of suppressing colorectal cancer ›Kenneth, W. K., et al., Science, 253, 661 (1991)! and the WTI gene capable of suppressing Wilms' tumor ›Call, K. M., et al., Cell, 60, 509 (1990)!. With respect to the p53 gene, cases are known in which germ-line mutations in the gene are inherited ›"LiFraumeni syndrome" (Makin, D., et al., Science, 250, 1233 (1990); and Srivastava, S., et al., Nature, 348, 747 (1990))!. It is gradually becoming apparent that defects in not only a single gene but also in multiple genes participate in the progression of the malignant phenotype of cancer, and it is believed that there will be further discovered a large number of unidentified oncogenes and tumor suppressor genes. Their discovery and
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elucidation are anticipated by not only research and clinical experts but also people worldwide. Web site: http://www.delphion.com/details?pn=US05935786__ ·
Methods for the early diagnosis of ovarian, breast and lung cancer Inventor(s): O'Brien; Timothy J. (Little Rock, AR) Assignee(s): The Board of Trustees of the University of Arkansas (Little Rock, AR) Patent Number: 6,316,213 Date filed: January 27, 2000 Abstract: The disclosed nucleic acid primer sets, used in combination with quantitative amplification (PCR) of tissue cDNA, can indicate the presence of specific proteases in a tissue sample. The detected proteases are themselves specifically overexpressed in certain cancers, and their presence may serve for early detection of associated ovarian and other malignancies, and for the design of interactive therapies for cancer treatment. Excerpt(s): Generally, the present invention relates to the fields of molecular biology and medicine. More specifically, the present invention is in the field of ovarian and other cancer diagnosis. To date, ovarian cancer remains the number one killer of women with gynecologic malignant hyperplasia. Approximately 75% of women diagnosed with such cancers are already at an advanced stage (III and IV) of the disease at their initial diagnosis. During the past 20 years, neither diagnosis nor five year survival rates have greatly improved for these patients. This is substantially due to the high percentage of high-stage initial detections of the disease. Therefore, the challenge remains to develop new markers that improve early diagnosis and thereby reduce the percentage of highstage initial diagnoses. Extracellular proteases have already been implicated in the growth, spread and metastatic progression of many cancers, due to the ability of malignant cells not only to grow in situ, but to dissociate from the primary tumor and to invade new surfaces. The ability to disengage from one tissue and re-engage the surface of another tissue is what provides for the morbidity and mortality associated with this disease. Therefore, extracellular proteases may be good candidates for markers of neoplastic development. Web site: http://www.delphion.com/details?pn=US06316213__
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Optical projection imaging system and method for automatically detecting cells having nuclear and cytoplasmic densitometric features associated with disease Inventor(s): Nelson; Alan C. (1509 56th Ave. Ct. NW., Gig Harbor, WA 98335) Assignee(s): none reported Patent Number: 6,519,355 Date filed: January 22, 2002 Abstract: A system and method for rapidly detecting cells of interest using multidimensional, highly quantitative, nuclear and cytoplasmic densitometric features (NDFs and CDFs) includes a flow optical tomography (FOT) instrument capable of generating various optical projection images (or shadowgrams) containing accurate density information from a cell, a computer and software to analyze and reconstruct the projection images into a multi-dimensional data set, and automated feature collection
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and object classifiers. The system and method are particularly useful in the early detection of cancers such as lung cancer using a bronchial specimen from sputum or cheek scrapings and cervical/ovarian cancer using a cervical scraping, and the system can be used to detect rare cells in specimens including blood. Excerpt(s): The present invention relates to projection imaging systems in general and cell classification, and more particularly, to high throughput flow based automated systems using projection imaging, such as flow optical tomography (FOT), for detecting abnormal and malignant cells and for detecting rare cells based on highly quantative measurements of nuclear and cytoplasmic densitometric features (NDFs and CDFs) associated with disease. The most common method of diagnosing cancer in patients is by obtaining a sample of the suspect tissue and examining it under a microscope for the presence of obviously malignant cells. While this process is relatively easy when the anatomic location of the suspect tissue is known, it is not so easy when there is no readily identifiable tumor or pre-cancerous lesion. For example, to detect the presence of lung cancer from a sputum sample requires one or more relatively rare cancer cells to be present in the sample. Therefore, patients having lung cancer may not be diagnosed properly if the sample does not perceptively and accurately reflect the conditions of the lung. One example of a microscope-based system and method for detecting diagnostic cells and cells having malignancy-associated changes is disclosed in Palcic et al., U.S. Pat. No. 6,026,174. The Palcic et al. system includes an automated classifier having a conventional microscope, camera, image digitizer, a computer system for controlling and interfacing these components, a primary classifier for initial cell classification, and a secondary classifier for subsequent cell classification. The method utilizes the automated classifier to automatically detect diagnostic cells and cells having malignancy-associated changes. However, the quality of the diagnostic result is limited by the use of a conventional microscope, which does not permit accurate measurement of stain densities. The method of Palcic et al. does not address the use of molecular probes. Web site: http://www.delphion.com/details?pn=US06519355__ ·
Pharmaceutical compositions, methods, and kits for treatment and diagnosis of lung cancer Inventor(s): Manyak; Michael J. (Chevy Chase, MD), Patierno; Steven R. (Falls Church, VA) Assignee(s): George Washington University (Washington, DC) Patent Number: 6,509,316 Date filed: December 9, 1997 Abstract: The present invention relates to pharmaceutical compositions, methods and kits that provide for the early diagnosis and treatment of lung cancer. More particularly, the present invention relates to pharmaceutical compositions containing uteroglobin for preventing or inhibiting metastasis of lung tumor cells and methods of using the same to prevent or inhibit metastasis of lung tumor cells. The present invention also relates to methods and kits for early diagnosis of metastatic lung cancer by assaying for uteroglobin and comparing the results against control cells. The present invention also relates to methods and kits for detection of metastatic lung cancer by assaying for the presence of an aberrant form of uteroglobin. Excerpt(s): The present invention relates to pharmaceutical compositions, methods and kits that provide for the early diagnosis and treatment of lung cancer. More particularly,
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the present invention relates to pharmaceutical compositions containing uteroglobin for treating or inhibiting metastasis of lung epithelial tumor cells and methods of using the same to treat or inhibit metastasis of lung epithelial tumor cells. The present invention also relates to methods and kits for early diagnosis of metastatic lung cancer by assaying for uteroglobin and comparing the results against control cells. Cancers develop from uncontrolled multiplication of cells. All cancers are life threatening, and lung cancer remains the major cause of cancer death among both males and females. There are four types of lung cancer found in humans: squamous, adeno, small cell, and large cell. Each tumor expresses specific differentiation features or surface phenotype determinants, all of which distinguish these cells form normal cells. The development of monoclonal antibody diagnostic techniques has greatly enhanced the production of reagents capable of differentiating normal cells from cancer cells and differentiating between cancer cell types. However, none of these markers have been able to provide information concerning when a tumor cell or cells will become metastatic. Web site: http://www.delphion.com/details?pn=US06509316__ ·
Proteins for cancer cell specific induction of apoptosis and method for isolation thereof Inventor(s): Tsai; David (2500 Townsgate Rd. Unit C, Westlake Village, CA 91361), Yu; Jenny (2500 Townsgate Rd. Unit C, Westlake Village, CA 91361) Assignee(s): none reported Patent Number: 5,994,298 Date filed: September 8, 1998 Abstract: The present invention provides the methods to isolate the proteins specifically induced apoptosis (programmed cell death) in prostate cancer cells (LNCAP), leukemia cells (HL-60), and breast cancer cells (MCF-70), but without effect in normal human lung fibroblast cells (CCD 39 Lu). P-1 has no effect on breast cancer cells. Five proteins have been isolated from the conditioned media of culture cells: (1) Apogen P-1: the proteins (Apogen P-1a, Apogen P-1b and Apogen P-1c) isolated from the conditioned medium of XC cells are able to induce apoptosis in prostate cancer cells (LNCAP) without effect in normal human lung fibroblast (CCD 39 Lu), colon cancer (T84), breast cancer (MCF-7) and leukemia (HL-60) cells. (2) Apogen P-2: the protein isolated from the conditioned medium of C3H10T1/2 cells is able to induce apoptosis in prostate cancer cells (LNCAP) and breast cancer (MCF-7) without effect in normal human lung fibroblast (CCD 39 Lu) and colon cancer (T84) cells. (3) Apogen L: the protein isolated from the conditioned medium of XC cells is able to induce apoptosis in leukemia cells (HL-60), and breast cancer (MCF-7) without effect in normal human lung fibroblast (CCD 39 Lu), colon cancer (T84) and prostate cancer (LNCAP) cells. The isolated protein Apogen P-2 is at least in part comprised of bovine fetuin. When properly prepared, fetuin is able to induce apoptosis in leukemia cells (HL-60), prostate cancer (LNCaP and PC-3) cells, colon cancer (Colo 205) cells, breast cancer (MCF-7) cells, and lung cancer (Calu-1) cells. The invention may lead to the discovery of a novel class of anticancer drug that aims at prostate cancer, breast cancer, leukemia and other cancers by inducing apoptosis in cancer cells without affecting normal cells. Excerpt(s): Human beings have had a long battle against cancer. Because the disease is so widespread, manifests itself in so many different ways and is so relentless, the potential market for effective cancer therapies is enormous. It is estimated that 10 million people in the U.S. either have or have had cancer. The National Cancer Institute
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(NCI) projects that in 1995, some 1.2 million new cases of cancer will be diagnosed in the United States, and that 538,000 people will die of the disease. Cancer is currently treated, with a low degree of success, with combinations of surgery, chemotherapy and radiation. The reason of the low degrees of success in cancer chemotherapy is as the following: Current chemotherapeutic approaches target rapidly dividing tumor cells. This approach is ineffective when the cancer is dormant or growing slowly. Such treatments also affect other, noncancerous cells that divide rapidly, causing harmful side effects. Only in the last several years has a new approach emerged in the battle against cancer. This approach is based on the newly discovered biological phenomenon called "Apoptosis". Apoptosis is also called "programmed cell death" or "cell suicide". (Krammer, et al., "Apoptosis in the APO-1 System", Apoptosis: The molecular Basis of Cell Death, pp. 87-99 Cold Spring Harbor Laboratory Press, 1991). In contrast to the cell death caused by cell injury, apoptosis is an active process of gene-directed, cellular selfdestruction and that it serves a biologically meaningful function. (Kerr, J. F. R and J. Searle J. Pathol. 107:41, 1971). One of the examples of the biologically meaningful functions of apoptosis is the morphogenesis of embryo. (Michaelson, J. Biol. Rev. 62:115, 1987). Just like the sculpturing of a sculpture, which needs the addition as well as removal of clay, the organ formation (Morphogenesis) of an embryo relies on cell growth (addition of clay) as well as cell death (removal of clay). As a matter of fact, apoptosis plays a key role in the human body from the early stages of embryonic development through to the inevitable decline associated with old age. (Wyllie, A. H. Int. Rev. Cytol. 68:251, 1980). The normal function of the immune, gastrointestinal and hematopoietic system relies on the normal function of apoptosis. When the normal function of apoptosis goes awry, the cause or the result can be one of a number of diseases, including: cancer, viral infections, auto-immune disease/allergies, neurodegeneration or cardiovascular diseases. Because of the versatility of apoptosis involved in human diseases, apoptosis is becoming a prominent buzzword in the pharmaceutical research field. Huge amounts of time and money are being spent in an attempt to understand how it works, how it can be encouraged or Inhibited and what this means for practical medicine. A handful of companies have been formed with the prime direction of turning work in this nascent field into marketable pharmaceutical products. The emergence of a core of innovative young companies combined with the tentative steps being taken by established industrial players are certain to make apoptosis research one of the fastest-growing and most promising areas of medical study of the 1990s. The idea that cancer may be caused by insufficient apoptosis merged only recently (Cope, F. O and Wille, J. j, "Apoptosis": The Molecular Basis of Cell Death, Cold Spring Harbor Laboratory Press, p. 61, 1991). This idea however, opens a door for a new concept in cancer therapy--Cancer cells may be killed by encouraging apoptosis. Apoptosis modulation, based on the processes present in normal development, is a potential mechanism for controlling the growth of tumor cells. Restoring apoptosis in tumor cells is an attractive approach because, at least in theory, it would teach the cells to commit suicide. Nevertheless, since the objective of cancer treatment is to kill cancer cells without killing the host, although apoptosis may open a new door for cancer therapy by inducing apoptosis in tumor cells, the success of this treatment is still dependent on the availability of drugs that can selectively induce apoptosis in tumor cells without affecting normal cells. In this patent application, we described the methods for the Isolation of proteins that specifically induce apoptosis in cancer cells without effect in normal cells. These proteins may present a new class of anticancer drugs that induce apoptosis in cancer cells which may offer a breakthrough in cancer therapy. Web site: http://www.delphion.com/details?pn=US05994298__
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Purified compositions of 10-propargyl-10-deazaaminopterin and methods of using same in the treatment of tumors Inventor(s): Sirotnak; Francis M. (New York, NY), Piper; James R. (Birmingham, AL), DeGraw; Joseph I. (Missoula, MT), Colwell; William T. (Menlo Park, CA) Assignee(s): Southern Research Institute (Birmingham, AL), SRI International (Menlo Park, CA), Sloan-Kettering Institute for Cancer Research (New York, NY) Patent Number: 6,028,071 Date filed: March 8, 1999 Abstract: Highly purified 10-propargyl-10-deazaaminopterin (10-propargyl-10dAM) compositions tested in xenograft models for their efficacy against human tumors are shown to be far superior to methotrexate ("MTX") and are even superior to the newer clinical candidate edatrexate ("EDX"). Moreover, 10-propragyl-10dAM showed a surprising ability to cure tumors such that there was no evidence of tumor growth several weeks after the cessation of therapy. Thus, highly purified compositions containing 10-propargyl-10dAM can be used to treat human tumors, particularly human mammary tumors and human lung cancer. Excerpt(s): This application relates to a purified composition of the compound 10propargyl-10-deazaaminopterin and to methods of using this compound in the treatment of tumors. Surprisingly, however, more highly purified 10-propargyl-10dAM compositions when tested in a xenograft model for their efficacy against human tumors have now been shown to be far superior to methotrexate ("MTX") and are even superior to edatrexate ("ETX"), a more recent clinical candidate. Moreover, 10-propargyl-10dAM showed a surprising ability to cure tumors such that there was no evidence of tumor growth several weeks after the cessation of therapy. Thus, a first aspect of the present invention is a highly purified composition containing 10-propargyl-10dAM. This composition can be used in accordance with the invention to treat tumors, particularly human mammary tumors and human lung cancer. This application relates to "highly purified" 10-propargyl-10dAM. As used in the specification and claims hereof, compositions which are "highly purified" contain 10-propargyl-10dAM substantially free of other folic acid derivatives particularly 10-deazaaminopterin, which can interfere with the antitumor activity of the 10-propargyl-10dAM. A composition within the scope of the invention may include carriers or excipients for formulating the 10-propargyl10dAM into a suitable dosage unit form for therapeutic use. Web site: http://www.delphion.com/details?pn=US06028071__
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Reagents and methods useful for detecting diseases of the lung Inventor(s): Roberts-Rapp; Lisa (Gurnee, IL), Klass; Michael R. (Libertyville, IL), Hodges; Steven C. (Buffalo Grove, IL), Stroupe; Steven D. (Libertyville, IL), Russell; John C. (Kenosha, WI), Friedman; Paula N. (Deerfield, IL), Cohen; Maurice (Highland Park, IL), Kratochvil; Jon D. (Kenosha, WI), Gordon; Julian (Lake Bluff, IL) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 5,939,265 Date filed: November 5, 1997 Abstract: A set of contiguous and partially overlapping RNA sequences and polypeptides encoded thereby, designated as LU103 and transcribed from lung tissue is
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described. A fully sequenced clone representing the longest continuous sequence of LU103 is also disclosed. These sequences are useful for detecting, diagnosing, staging, monitoring, prognosticating, preventing or treating, or determining the predisposition of an individual to diseases and conditions of the lung such as lung cancer. Excerpt(s): The invention relates generally to detecting diseases of the lung. More particularly, the invention relates to reagents such as polynucleotide sequences and the polypeptide sequences encoded thereby, as well as methods which utilize these sequences. The polynucleotide and polypeptide sequences are useful for detecting, diagnosing, staging, monitoring, prognosticating, preventing or treating, or determining predisposition to diseases or conditions of the lung such as lung cancer. Lung cancer is the second most common cancer for both men and women in the United States, with an estimated 178,100 newly diagnosed during 1997 (American Cancer Society statistics). It also is the most common cause of cancer death for both sexes, with over 160,000 lung cancer related deaths expected in 1997. Lung cancer is a major health problem in other areas of the world, with approximately 135,000 new cases occurring each year in the European Union, and its incidence rapidly increasing in Central and Eastern Europe. See, Genesis Report, February 1995 and T. Reynolds, J. Natl. Cancer Inst. 87: 1348-1349 (1995). Early stage lung cancer can be detected by chest radiograph and the sputum cytological examination; however, these procedures do not have sufficient sensitivity for routine use as screening tests for asymptomatic individuals. Potential technical problems which can limit the sensitivity of chest radiograph include suboptimal technique, insufficient exposure, and positioning and cooperation of the patient. T. G. Tape et al., Ann. Intern. Med. 104: 663-670 (1986). Moreover, radiologists often disagree on interpretations of chest radiographs; over 40% of these disagreements are significant or potentially significant, with false-negative interpretations being the cause of most errors. P. G. Herman et al., Chest 68: 278-282 (1975). Inconclusive results require additional follow-up testing for clarification. T. G. Tape et al., supra. Sputum cytology is even less sensitive than chest radiography in detecting early lung cancer; of 160 lung cancer cases, radiography alone detected 123 cases (77%) while cytological examination alone detected 67 cases (42%). The National Cancer Institute "Early Lung Cancer Detection: Summary and Conclusion," Am. Rev. Resp. Dis. 130: 565-567 (1984). Factors affecting the ability of sputum cytological examination to diagnose lung cancer include the ability of the patient to produce sufficient sputum, the size of the tumor, the proximity of the tumor to major airways, the histologic type of the tumor, and the experience and training of the cytopathologist. R. J. Ginsberg et al. In: Cancer: Principles and Practice of Oncology, Fourth Edition, V. T. DeVita, S. Hellman, S. A. Rosenburg, pp. 673-723, Philadelphia, Pa.: J. B. Lippincott Co. (1993). Web site: http://www.delphion.com/details?pn=US05939265__ ·
System and method for detection of a biological condition Inventor(s): Berry; Michael J. (Carmel, CA) Assignee(s): Quadrivium, L.L.C. (Phoenix, AZ) Patent Number: 6,363,772 Date filed: December 10, 1999 Abstract: A system and method that allows for early detection of biological conditions, such as a disease, through analysis of appropriate gaseous samples. The system and method are particularly amenable to the early screening for diseases, such as lung cancer, through the detection of specific biomarkers when present in exhaled breath
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from an individual. A preferred system implements a CO overtone laser that generates radiation and directs it through a photoacoustic cell. The absorption of the radiation is detected acoustically, and the absorption characteristics are utilized in determining the presence of a specific biological condition. Excerpt(s): The present invention relates generally to the detection of volatile organic compounds that serve as biomarkers for a biological condition, such as a disease, and particularly to a noninvasive system and method for determining the presence of such condition in an individual or substance through analysis of a gaseous sample from the individual or substance. Early detection of disease in an individual is often important to successful treatment of that disease. A variety of techniques are used to test for specific diseases either before or after symptoms occur. For example, blood samples and urine samples are routinely taken for analysis and detection of abnormalities indicative of disease. Many of these techniques are invasive or uncomfortable for the patient. One potential noninvasive technique for determining the presence of a variety of diseases in the body of an individual is breath analysis. There are over three hundred distinct chemical compounds that may be detected in human expired breath, and each of these distinct chemical compounds has its own absorption spectrum. Studies have shown that specific alterations or changes in this expired air are indicative of specific diseases. This is true for some diseases because of the direct compositional relationship between constituents carried in the blood stream and constituents excreted into the alveolar spaces of the lungs. In any event, the changes or alterations in the constituents of an individual's breath can be detected to determine whether the individual has a particular biological condition, such as a disease or metabolic disorder. Web site: http://www.delphion.com/details?pn=US06363772__ ·
Use of betulinic acid derivatives for inhibiting cancer growth Inventor(s): Ramadoss; Sunder (Delhi, IN), Siddiqui; Mohammad Jamshed Ahmed (Ghaziabad, IN), Khanna; Achla B. (Delhi, IN), Jaggi; Manu (Haryana, IN) Assignee(s): Dabur Research Foundation (Ghaziabad, IN) Patent Number: 6,214,814 Date filed: February 17, 1999 Abstract: The invention relates to the use of betulinic acid and its derivatives for the inhibition and/or prevention or cancer growth. The invention also relates to novel betulinic acid derivatives useful for the inhibition of tumor/cancer cells and a process for the preparation of the derivatives. The invention also relates to the antileukemic, and anti-lymphoma activity of the betulinic acid derivatives, and the use of the derivatives for the treatment of prostate, ovarian and lung cancer. Excerpt(s): The invention relates to the use of betulinic acid and its derivatives for the inhibition and/or prevention or cancer growth. The invention also relates to novel betulinic acid derivatives useful for the inhibition of tumor/cancer cells and a process for the preparation of the derivatives. The invention also relates to the antileukemic, and anti-lymphoma activity of the betulinic acid derivatives, and the use of the derivatives for the treatment of prostate, ovarian and lung cancer. Under the auspices of a National Cooperative Natural Product Drug Discovery Group supported by the National Cancer Institute, the potential antitumor activity of approximately 2500 extracts derived from globally collected plants was evaluated in a panel of enzyme based assays and in a battery of cultured human tumor cell lines. One such extract, prepared from the stem
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bark of Ziziphus mauritiana Lam. (Rhamnaceae), displayed selective cytotoxicity against cultured human melanoma cells (Nature Medicine, Vo. 1 (10), 1995, WO 96/29068). As a result of bioactivity guided fractionation, betulinic acid, a pentacyclic triterpene, was identified as a melanoma-specific cytotoxic agent. In follow-up studies conducted with a thymic mice carrying human melanomas, tumor growth was completely inhibited without toxicity. As judged by a variety of cellular responses, antitumor activity was mediated by the induction of apoptosis. A number of triterpenoids, including betulinic acid, have several known medical applications, including use as anticancer drugs. Anderson et al., in WO 95/04526, have discussed the derivatives of triterpenoids which have been used in cancer therapy, including their activity against polyamines which are required by cells to grow at an optimal rate. Some of these triterpenoids have been found to interfere with enzymatic synthesis of polyamines required for optimal cell growth, and thus inhibit the growth of cancer cells, particularly by inhibiting ornithine decarboxylase (Yasukawa, K. et al., Oncology 48: 7276, 1991), The anti-cancer activity of betulinic acid and some derivatives has been demonstrated using mouse sarcoma 180 cells implanted subcutaneously in nude mice (JP 87,301,580). Choi et al have shown that betulinic acid 3-monoacetate, and betulinic acid methyl ester exhibit ED.sub.50 values of 10.5 and 6.8.mu.g/ml, respectively, against p388 lymphocytic leukemia cells (Choi, Y-H et al., Planta Medical vol. XLVII, pages 511513, 1988). Web site: http://www.delphion.com/details?pn=US06214814__
Patent Applications on Lung Cancer As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to lung cancer: ·
21910, a novel human membrane-associated guanylate kinase and uses thereof Inventor(s): Kapeller-Libermann, Rosana; (Chestnut Hill, MA), Hunter, John Joseph; (Somerville, MA) Correspondence: LAHIVE & COCKFIELD; 28 STATE STREET; BOSTON; MA; 02109; US Patent Application Number: 20030108934 Date filed: October 22, 2002 Abstract: The invention provides isolated nucleic acid molecules, designated MAGK nucleic acid molecules, which encode novel guanylate kinase related molecules. The invention also provides antisense nucleic acid molecules, recombinant expression vectors containing MAGK nucleic acid molecules, host cells into which the expression vectors have been introduced, and nonhuman transgenic animals in which a MAGK gene has been introduced or disrupted. The invention still further provides isolated MAGK proteins, fusion proteins, antigenic peptides and anti-MAGK antibodies. Treatment and diagnostic methods for cellular growth or proliferation diseases or disorders, e.g., cancer, including, but not limited to colon cancer and lung cancer, utilizing compositions of the invention, are also provided.
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This has been a common practice outside the United States prior to December 2000.
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Excerpt(s): This application claims the benefit of prior-filed provisional patent application Serial No. 60/205,447, filed May 19, 2000, entitled "21910, A Novel Human Membrane-Associated Guanylate Kinase and Uses Thereof". The entire content of the above-referenced application is incorporated herein by this reference. Guanylate kinases are essential enzymes in nucleotide metabolism pathways catalyzing the ATPdependent phosphorylation of either GMP to GDP or dGMP to dGDP. Guanyate kinase molecules also function in the recovery of cGMP (cGMP.fwdarw.GMP.fwdarw.GDP.fwdarw.GTP.fwdarw.cGMP) thereby serving to regulate the supply of guanine nucleotides to signal transduction pathway components (Brady et al. (1996) J. Biol. Chem. 271(28):16734-40; Kumar, et al. (2000) Eur. J. Biochem. 267(2):606). Guanylate kinases are essential to a wide range of cellular processes including but not limited to nucleotide metabolic processes (e.g., supplying the building blocks for nucleic acids), phototransduction processes (e.g., regulating the opening and/or closing of cGMP gated-channels), cellular growth and proliferation, and signaling pathways (Fitzgibbon, et al (1996) FEBS Letters 385:185-188). Membranebound forms of guanylate kinase molecules have also been discovered. Members of the membrane-associated guanylate kinase family interact with the cytoskeleton of the cell and regulate cell proliferation, signaling pathways, and intercellular junctions. (Kim, et al. (1996) Genomics 31(2):223). These molecules participate in the assembly of multiprotein complexes on the inner surface of the plasma membrane and cluster ion channels, receptors, adhesion molecules and cytosolic signaling proteins at synapses, cellular junctions, and polarized membrane domains (Fannin and Anderson (1999) Curr. Opin. Cell Biol. 11(4):432; Dobrosotskaya, et al. (1997) J. Biol. Chem. 272(50):31589). In addition, membrane-associated guanylate kinases have recently been found to have a transcriptional regulatory function (Hsueh, et al. (2000) Nature 404(6775):298). Typically, these molecules contain multiple protein-protein interaction motifs including a PDZ domain in the N-terminal portion of the protein, followed by a SH3 domain, followed by a guanylate kinase domain at the C-terminus (Dobrosotskaya, et al., supra). Membrane-associated guanylate kinases have been found to be localized to tight junctions in epithelial cell membranes and more notably in neuronal cells (Wu, et al. (2000) Proc. Natl Acad. Sci. USA 97(8):4233); Hsuesh, supra). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
2-Methoxyestradiol-induced apoptosis in cancer cells Inventor(s): Mukhopadhyay, Tapas; (Houston, TX), Roth, Jack A.; (Houston, TX) Correspondence: Steven L. Highlander, Esq.; FULBRIGHT & JAWORSKI L.L.P.; Suite 2400; 600 Congress Avenue; Austin; TX; 78701; US Patent Application Number: 20030099614 Date filed: June 25, 2002 Abstract: The present invention details methods for the treatment of cancer. In particular, it concerns the induction of apoptosis of cancer cells following treatment with methoxyestradiol. 2-methoxyestradiol (2-MeOE.sub.2) increase wild-type p53 levels in a human non-small lung cancer cell lines associated with accumulation of cyclin dependent kinase inhibitor p21WAF1/CIP1. Significant apoptotic cell death occurred after the drug treatment. Thus, 2-MeOE.sub.2 facilitates induction of p53-mediated apoptosis. Excerpt(s): The present invention relates generally to the field of cancer therapy. More particularly, it concerns the use of methoxyestradiol to stimulate p53 expression in
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tumor cells, thereby inducing programmed cell death. Normal tissue homeostasis is achieved by an intricate balance between the rate of cell proliferation and the rate of cell death. Disruption of this balance is thought to be a major deleterious event in the development of cancer. The inhibition of apoptosis (programmed cell death) has been linked to this disruptive event. The effects of such defects are catastrophic, causing over half a million deaths per annum in the United States alone. The p53 gene is well recognized as a tumor suppressor gene (Montenarh, 1992). There is now considerable evidence linking mutations of p53 in the oncogenesis of many human cancers. There are numerous reports demonstrating that the growth of, for example, colon, glioblastoma, breast cancer, osteosarcoma and lung tumor cells can be suppressed by the expression of wild-type p53. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Angiotensin-(1-7) and angiotensin-(1-7) agonists for inhibition of cancer cell growth Inventor(s): Tallant, E. Ann; (Lewisville, NC), Gallagher, Patricia E.; (Lewisville, NC), Ferrario, Carlos M.; (Winston-Salem, NC) Correspondence: Cynthia B. Rothschild, Esq.; Kilpatrick Stockton LLP; 1001 West Fourth Street; Winston-Salem; NC; 27101-2400; US Patent Application Number: 20030203834 Date filed: February 27, 2003 Abstract: The present invention describes the use of angiotensin-(1-7) peptide as an anticancer therapeutic. Thus, in one embodiment, the present invention comprises a composition to inhibit the growth of cancer cells in an individual comprising a pharmaceutically effective amount of an agonist for the angiotensin-(1-7) receptor to inhibit cancer cell growth or proliferation. Application of a pharmaceutically effective amount of angiotensin-(1-7) or angiotensin-(1-7) receptor agonist is associated with an increase in the expression of genes involved in tumor suppression, apoptosis, and/or cell cycle inhibition, and a decrease the expression of known oncogenes, protein kinases, and/or cell cycle progression genes. Cancers treated using the methods and compositions described herein include cancers having an angiotensin-(1-7) receptor, including, but not limited to, breast and lung cancer. Excerpt(s): This application claims priority to U.S. Provisional Application Serial No. 60/359,847, filed Feb. 27, 2002. The disclosure of U.S. Provisional Application Serial No. 60/359,847 is incorporated herein by reference in its entirety. The present invention relates to compositions and methods for the treatment and prevention of cancer. More specifically, the present invention relates to the use of angiotensin-(1-7) or other agonists for the angiotensin-(l1-7) receptor as anticancer therapeutics. Angiotensin-(1-7) [Ang-(17)] is an endogenous peptide hormone which is normally present in the circulation at concentrations similar to angiotensin II (Ang II) and is primarily derived from angiotensin I (Ang I) by tissue peptidases, including neprilysin, thimet oligopeptidase and prolyl endopeptidase (Ferrario, C. M. et al., Hypertension, 1997, 30:535-541) and by angiotensin converting enzyme (ACE) 2 from angiotensin II (Ang II) (Vickers, C., et al., J. Biol. Chem., 2002, 277:14836-14843). In addition, Ang-(1-7) is a substrate for ACE (Chappell, M. C. et al. Hypertension, 1998, 31:362-367). ACE catalyzes the conversion of angiotensin I (Ang I) to the biologically active peptide angiotensin II [Ang II]. Treatment of patients or animals with ACE inhibitors results in a significant elevation in the circulating and tissue levels of Ang II, as well as the N-terminal heptapeptide fragment of Ang II, angiotensin-(1-7) (Campbell, M. C. et al., Hypertension, 1993, 22:513-522;
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Kohara, K. et al., Hypertension, 1991, 17:131-138; Lawrence, A. C. et al., J. Hypertens., 1990, 8:715-724; and Luque, M. et al., J. Hypertens., 1996, 14:799-805). It has been suggested that ACE inhibition not only elevates Ang-(1-7) by increasing Ang I, the substrate for Ang-(1-7) production, but also by preventing Ang-(1-7) conversion to the inactive fragment Ang-(1-5). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Aziridinyl quinone antitumor agents based on indoles and cyclopent[b]indoles Inventor(s): Skibo, Edward B.; (Mesa, AZ), Xing, Chengguo; (Somerville, MA) Correspondence: FENNEMORE CRAIG; 3003 NORTH CENTRAL AVENUE; SUITE 2600; PHOENIX; AZ; 85012; US Patent Application Number: 20030139609 Date filed: September 10, 2002 Abstract: A large number of aziridinyl quinones represented by Series 1-9 were studied with respect to their DT-diaphorase substrate activity, DNA reductive alkylation, cytostatic/cytotoxic activity, and in vivo activity. As a result generalizations have been made with respect with respect to the following: DT-diaphorase substrate design, DTdiaphorase-cytotoxicity QSAR, and DNA reductive alkylating agent design. A saturating relationship exists between the substrate specificity for human recombinant DT-diaphorase and the cytotoxicity in the human H460 non-small-cell lung cancer cell line. The interpretation of this relationship is that reductive activation is no longer rate limiting for substrates with high DT-diaphorase substrate specificities. High DTdiaphorase substrate specificity is not desirable in the indole and cylopent[b]indole systems because of the result is the loss of cancer selectivity along with increased toxicity. We conclude that aziridinyl quinones of this type should possess a substrate specificity (VMAX/KM )