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1. Genome-wide interaction study of smoking behavior and non-small cell lung cancer risk in Caucasian population

Author

Rayjean J. Hung, Vladimir Janout, Natasha B. Leighl, Geoffrey Liu, David C. Christiani, Kim Overvad, Beata Swiatkowska, Eric J. Duell, David C. Muller, Aage Haugen, Angeline S. Andrew, Jonas Manjer, Mattias Johansson, David Zaridze, Mikael Johansson, Simona Ognjanovic, Demetrios Albanes, H-Erich Wichmann, Jolanta Lissowska, Kjell Grankvist, Angela Cecilia Pesatori, David C. Qian, Younghun Han, Richard S. Houlston, Matthew B. Schabath, James D. McKay, Pier Alberto Bertazzi, Matt J. Barnett, Lambertus A. Kiemeney, Michael W. Marcus, Penella J. Woll, Gad Rennert, Tadeusz M Orlowski, Gary E. Goodman, Stephen Lam, Lesley M. Butler, Loic Le Marchand, Ciprian Bolca, Antonia Trichopoulou, Paul Brennan, Rosario Tumino, María Soler Artigas, Melinda C. Aldrich, Stig E. Bojesen, Ghislaine Scelo, Vidar Skaug, Xifeng Wu, Judith Manz, William S. Bush, Olle Melander, Olga Y. Gorlova, Susanne M. Arnold, Jakob S Johansen, Hans Brunnström, Xiangjun Xiao, Ivana Holcatova, John K. Field, Angela Risch, Philip Lazarus, Eric B. Haura, Anush Mukeria, Yafang Li, Angela Cox, Frances A. Shepherd, Neil E. Caporaso, Heike Bickeböller, Albert Rosenberger, Fiona Taylor, Shanbeh Zienolddiny, Milica Kontic, M. Dawn Teare, Per Bakke, Adonina Tardón, Chu Chen, Thomas Muley, Christopher I. Amos, Nofer Institute of Occupational Medicine, Biomedical Data Science Department, Dartmouth College, Hanover, NH, USA, Department of Medicine, The Princess Margaret Cancer Center, University Health Network, Toronto, ON, Canada, Department of Oncology, Herlev and Gentofte Hospital, Copenhagen University Hospital, Copenhagen University, Herlev, Denmark, Public Health Sciences Division, Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA, USA, Public Health Sciences Division, Cancer Prevention Program, Swedish Medical Center, Seattle, WA, USA, Department of Oncology, University of Sheffield, Sheffield UK, Institute of Epidemiology, Helmholtz Centre Munich, Neuherberg, Germany, Biobank and Tumor Documentation, Thoraxklinik at University Hospital Heidelberg, Heidelberg, Germany, Department of Genetic Epidemiology, Medical School, Georg-August University of Göttingen, Göttingen, Germany, Markey Cancer Center, University of Kentucky, Lexington, KY, USA, Department of Thoracic Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, USA, Thoracic Surgery Division, 'Marius Nasta' National Institute of Pneumology, București, Romania, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic, Internal Medicine, School of Medicine, Clinical Center of Serbia, University of Belgrade, Belgrade, Serbia, Department of Cancer Epidemiology and Prevention, M. Sklodowska-Curie Cancer Center, Institute of Oncology, Warsaw, Pol, Department of Epidemiology and Prevention, Russian N.N. Blokhin Cancer Research Centre, Moscow, Russia, International Organization for Cancer Prevention and Research, Belgrade, Serbia, Department of Thoracic Surgery, National Institute of Tuberculosis and Lung Diseases, Warsaw, Pol, International Agency for Research on Cancer (IARC), Genetic Epidemiology Group, Lyon, France, Department of Environmental Epidemiology, Nofer Institute of Occupational Medicine, Łódź, Pol, Department of Clinical Science, University of Bergen, Bergen, Norway, Department of Toxicology, National Institute of Occupational Health, Oslo, Norway, Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO-IDIBELL), Hospitalet de Llobregat, Barcelona, Spain, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA, The Institute of Cancer Research, London, UK, Department of Health Sciences, Genetic Epidemiology Group, University of Leicester, Leicester, UK, Department of Medical Biosciences, Umeå University, Umeå, Sweden, Department of Radiation Sciences, Umeå University, Umeå, Sweden, Medical Oncology Toronto, Princess Margaret Hospital, Toronto, ON, Canada, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK, Department of Clinical Sciences, Lund University, Lund, Sweden, Department of Internal Medicine, Skåne University Hospital, Malmö, Sweden, Department of Epidemiology and Biostatistics, Imperial College London, St Mary’s Campus, London, UK, Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus C, Denmark, Department of Hygiene and Epidemiology, Medical School, University of Athens, Athens, Greece, Molecular and Nutritional Epidemiology Unit, CSPO (Cancer Research and Prevention Centre), Scientific Institute of Tuscany, Florence, Italy, Princess Margaret Cancer Centre, Toronto, ON M5G, Canada, Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark, Department of Epidemiology, University of Texas MD Anderson Cancer Center, Houston, TX, USA, Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA, Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, MD, USA, Department of Genetic Epidemiology, University Medical Center, Georg-August University Göttingen, Göttingen, Germany, Department of Thoracic Surgery, Division of Epidemiology, Vanderbilt University Medical Center, Nashville, TN, USA, Department of Epidemiology and Biostatistics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA, Medicina, IUOPA-Universidad de Oviedo, Oviedo, Spain, Technion Faculty of Medicine, Clalit National Cancer Control Center, Carmel Medical Center, Haifa, Israel, Genetic Epidemiology, School of Health and Related Research, University of Sheffield, Sheffield, UK, Institute of Translational Medicine, University of Liverpool, Liverpool, UK, Department for Health Evidence, Radboud University Medical Center, Nijmegen EZ, Netherlands, Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Spokane, WA, USA, Department of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA, Department of Epidemiology, Norris Cotton Cancer Center, Dartmouth College, Hanover, NH, USA, Department of Preventive Medicine, IRCCS Foundation Cà Granda Ospedale, Maggiore Policlinico, University of Milan, Milan, Italy, Department of Clinical Sciences and Community Health–DISCCO, University of Milan, Milan, Italy, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, International Agency for Research on Cancer, World Health Organization, Lyon, France, and Division of Epidemiology, Dalla Lana School of Public Health, University of Toronto, Lunenfeld-Tanenbaum Research Institute, Toronto, Ontario, Canada

Subjects
0301 basic medicine, Cancer Research, Carcinogenesis, Population, Genome-wide association study, Single-nucleotide polymorphism, Bioinformatics, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, Hàbit de fumar, 0302 clinical medicine, Missing heritability problem, Genotype, Journal Article, medicine, Carcinogènesi, Oncology & Carcinogenesis, Lung cancer, education, education.field_of_study, business.industry, Smoking, Case-control study, General Medicine, Odds ratio, medicine.disease, 3. Good health, 030104 developmental biology, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], 030220 oncology & carcinogenesis, Càncer de pulmó, business, 1112 Oncology And Carcinogenesis
Abstract

Non-small cell lung cancer is the most common type of lung cancer. Both environmental and genetic risk factors contribute to lung carcinogenesis. We conducted a genome-wide interaction analysis between single nucleotide polymorphisms (SNPs) and smoking status (never-versus ever-smokers) in a European-descent population. We adopted a two-step analysis strategy in the discovery stage: we first conducted a case-only interaction analysis to assess the relationship between SNPs and smoking behavior using 13 336 non-small cell lung cancer cases. Candidate SNPs with P-value

Published
2017
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2. International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants

Author

Behnaz Pezeshki Naeim, Heike Bickeböller, James McKay, Vladimir Janout, Chikako Kiyohara, Shanbeh Zienolddiny, Aage Haugen, Eric J. Duell, Angeline S. Andrew, Joshua E. Muscat, Neonilia Szeszenia-Dabrowska, Ying Wang, Hendrik Dienemann, Michael J. Thun, Rayjean J. Hung, Jolanta Lissowska, Vladimir Bencko, Maria Teresa Landi, Keitaro Matsuo, Marcin Lener, Hongbing Shen, Angela Risch, Thomas Illig, Joanna Trubicka, Daniel P.K. Ng, Neil E. Caporaso, Margaret R. Spitz, H. Dean Hosgood, Paul Brennan, Jin Hee Kim, Philip Lazarus, Qing Lan, Adeline Seow, Eleonora Fabianova, Yun Chul Hong, Demetrius Albanes, Paolo Boffetta, Loic Le Marchand, Jan Lubinski, H.-Erich Wichmann, Takeshi Suzuki, Ping Yang, Zuo-Feng Zhang, Vali Constantinescu, Amelie Chabrier, Christopher I. Amos, Peter Rudnai, Lenka Foretova, Wiebke Sauter, Thérèse Truong, Carla J. Gallagher, David Zaridze, Truong, T., Sauter, W., McKay, J.D., Hosgood III, D.H., Gallagher, C., Amos, C.I., Spitz, M., Muscat, J., Lazarus, P., Illig, T., Wichmann, H.E., Bickeböller, H., Risch, A., Dienemann, H., Zhang, Z.-F., Naeim, B.P., Yang, P., Zienolddiny, S., Haugen, A., Marchand, L.L., Hong, Y.-C., Kim, J.H., Duell, E.J., Andrew, A.S., Kiyohara, C., Shen, H., Matsuo, K., Suzuki, T., Seow, A., Ng, D.P., Lan, Q., Zaridze, D., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Constantinescu, V., Bencko, V., Foretova, L., Janout, V., Caporaso, N.E., Albanes, D., Thun, M., Landi, M.T., Trubicka, J., Lener, M., Lubinski, J., Wang, Y., Chabrier, A., Boffetta, P., Brennan, P., and Hung, R.J.

Subjects
Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Candidate gene, Lung Neoplasms, Genotype, Genome-wide association study, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Odds Ratio, medicine, Humans, Genetic Predisposition to Disease, Lung cancer, Methylenetetrahydrofolate Reductase (NADPH2), Aged, 030304 developmental biology, Molecular Epidemiology, 0303 health sciences, biology, Lung Cancer, Intracellular Signaling Peptides and Proteins, Cancer, General Medicine, Odds ratio, Middle Aged, medicine.disease, susceptibility variant, Lung cancer susceptibility, 3. Good health, 030220 oncology & carcinogenesis, Methylenetetrahydrofolate reductase, Immunology, biology.protein, Female, Tumor Suppressor p53-Binding Protein 1, Consortium, Genome-Wide Association Study, Molecular Chaperones
Abstract

Background: Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancerrelated pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods: Genotype data from 15 ILCCO case-control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results: Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10-4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89-0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85-0.95), P = 1 × 10-4]. Conclusion: This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.

Published
2010
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3. CYP450 polymorphisms as risk factors for early-onset lung cancer: gender-specific differences

Author

Heinz-Erich Wichmann, Jenny Chang-Claude, Albert Rosenberger, Heike Bickeböller, Helmut Bartsch, Thomas Illig, Kirstin Mittelstrass, Angela Risch, Maria Timofeeva, Wiebke Sauter, Hendrik Dienemann, Birgit Jäger, Silke Kropp, and Lars Beckmann

Subjects
Adult, Male, Oncology, Cancer Research, medicine.medical_specialty, Lung Neoplasms, Single-nucleotide polymorphism, Biology, 03 medical and health sciences, Sex Factors, 0302 clinical medicine, Cytochrome P-450 Enzyme System, Risk Factors, Internal medicine, Genotype, medicine, Humans, Genetic Predisposition to Disease, Age of Onset, Lung cancer, 030304 developmental biology, 0303 health sciences, Smoking, Respiratory disease, Haplotype, Cancer, General Medicine, Odds ratio, Middle Aged, medicine.disease, 3. Good health, Minor allele frequency, Case-Control Studies, 030220 oncology & carcinogenesis, Immunology, Female, Precancerous Conditions
Abstract

Cytochrome P450 (CYP) enzymes, involved in metabolism of tobacco carcinogens, are also involved in estrogen metabolism and many are regulated by estrogens. These genes may thus be of relevance to gender-specific differences in lung cancer risk, particularly in early-onset lung cancer, where a high proportion of women is observed. We conducted a case-control study to investigate genetic polymorphisms in cytochromes that might modify the risk of developing early-onset lung cancer. In total, 638 Caucasian patients under the age of 51 with primary lung cancer and 1300 cancer-free control individuals, matched by age and sex, were included in this analysis. Thirteen polymorphisms in the CYP1A1, CYP1B1, CYP2A13, CYP3A4 and CYP3A5 genes were analyzed. No significant association was found for any of the analyzed polymorphisms and lung cancer risk overall. However, among women, a significantly increased risk of early-onset lung cancer was observed for carriers of the minor allele of CYP1B1 SNP rs1056836 [odds ratio (OR) 1.97; 95% confidence interval (CI) 1.32-2.94; P < 0.001]. Also, a non-significant increase in lung cancer risk was observed in the group of women carriers of the minor allele of CYP2A13 SNP rs1709084 (OR 1.64; 95% CI 1.00-2.70; P = 0.05). The effect of these two polymorphisms was shown to be modified by smoking. Haplotype analysis was performed for CYP1B1 and CYP2A13. No differences between cases and controls were observed for both genes (P = 0.63 and P = 0.42 for CYP1B1 and CYP2A13, respectively). Our results suggest that the CYP1B1 and the CYP2A13 genotypes may contribute to individual susceptibility to early-onset lung cancer in women.

Published
2009
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4. Comparison of multiple DNA adduct types in tumor adjacent human lung tissue: effect of cigarette smoking

Author

Angela Risch, Roger W. L. Godschalk, Klaus Kayser, Peter Drings, Hendrik Dienemann, F.J. van Schooten, Jagadeesan Nair, H Bartsch, Gezondheidsrisico Analyse en Toxicologie, and RS: NUTRIM School of Nutrition and Translational Research in Metabolism

Subjects
Male, Cancer Research, Pathology, medicine.medical_specialty, Lung Neoplasms, Time Factors, DNA damage, medicine.disease_cause, Deoxycytidine, Tobacco smoke, Lipid peroxidation, DNA Adducts, chemistry.chemical_compound, DNA adduct, medicine, Humans, Lung cancer, Carcinogen, Aged, Deoxyadenosines, Chemistry, Smoking, General Medicine, Middle Aged, medicine.disease, Molecular biology, Hydrocarbons, Nitrosamine, Female, Carcinogenesis, DNA Damage, Thymidine
Abstract

Comparison of multiple DNA adduct types in tumor adjacent human lung tissue: effect of cigarette smoking.Godschalk R, Nair J, van Schooten FJ, Risch A, Drings P, Kayser K, Dienemann H, Bartsch H.German Cancer Research Center (DKFZ), Division of Toxicology and Cancer Risk Factors, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.Cigarette smokers inhale a broad range of carcinogens derived from tobacco and its pyrolysis products, including free radicals, which induce oxidative stress and subsequent lipid peroxidation (LPO). Miscoding carcinogen-DNA adducts are formed by cigarette smoke constituents and are thought to initiate lung carcinogenesis. The presence of various types of DNA damage was therefore analyzed in tumor adjacent uninvolved lung tissues of 13 smoking and 11 non-smoking operated lung cancer patients. O(4)-ethylthymidine (O(4)etT), 1,N(6)-ethenodeoxyadenosine ( epsilon dA) and 3,N(4)-ethenodeoxycytidine ( epsilon dC) were determined by immuno-enriched (32)P-postlabeling. Polycyclic aromatic hydrocarbon (PAH)-DNA adducts were measured as diagonal radioactive zones after nuclease P1 enriched (32)P-postlabeling. Mean O(4)etT and PAH-DNA adduct levels were higher in lung DNA of smokers than of non-smokers (O(4)etT/10(8) thymidine: 3.8 versus 1.6, P < 0.01; PAH-DNA adducts/10(8) nucleotides: 11.2 versus 2.2, P < 0.01). Pulmonary etheno-DNA adduct levels did not differ between smokers and non-smokers, but large inter-individual variations were observed (80- and 250-fold differences for epsilon dA and epsilon dC, respectively). As all smokers (except one) refrained from smoking at least for 1 week before surgery, our results demonstrate the persistence of O(4)etT and PAH-DNA adducts in human lung. A positive correlation obtained between O(4)etT and PAH-DNA adducts (R = 0.65, P < 0.01) suggests that both adducts are formed from cigarette smoke as the main exposure source. We conclude that in addition to the DNA adducts derived from PAH and tobacco-specific nitrosamines, miscoding O(4)etT lesions are formed by cigarette smoke that contribute to the increased genomic instability and increased lung cancer risk in smokers

Published
2002
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5. Pleiotropic Analysis of Lung Cancer and Blood Triglycerides

Author

Jacqueline de Graaf, Nilanjan Chatterjee, Demetrius Albanes, Ite A. Laird-Offringa, Richard S. Houlston, James McKay, Victoria L. Stevens, Marina Laplana, Ole A. Andreassen, Lambertus A. Kiemeney, Andrew J. Schork, Verena Zuber, Maria Teresa Landi, Dorine W. Swinkels, Rayjean J. Hung, Lei Song, Chenchen Yang, Henricus F. M. van der Heijden, Srdjan Djurovic, Beiyun Zhou, Younghun Han, Angela Risch, William Wheeler, Jose I. Mayordomo, Yongyue Wei, Heike Bikeböller, Ian G. Mills, Aree Witoelar, Yunpeng Wang, Francesco Bettella, Maria Angeles Panadero, Katja K.H. Aben, Crystal N. Marconett, David C. Christiani, Zea Borok, Christopher I. Amos, Jianxin Shi, Xing Hua, Anders M. Dale, Wesley K. Thompson, and Neil E. Caporaso

Subjects
0301 basic medicine, Oncology, Cancer Research, Pathology, Lung Neoplasms, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], Blood lipids, Genome-wide association study, Type 2 diabetes, VARIANTS, DISEASE, Risk Factors, 2.1 Biological and endogenous factors, Aetiology, Lung, Cancer, RISK, 2. Zero hunger, Genetic Pleiotropy, Single Nucleotide, 3. Good health, Phenotype, Cardiovascular Diseases, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], Chromosomes, Human, Pair 6, Pair 6, Lung cancer, Brief Communications, Life Sciences & Biomedicine, Rare cancers Radboud Institute for Health Sciences [Radboudumc 9], Human, medicine.medical_specialty, Oncology and Carcinogenesis, IMMUNITY, Biology, Polymorphism, Single Nucleotide, Chromosomes, 03 medical and health sciences, INFLAMMATION, SDG 3 - Good Health and Well-being, Meta-Analysis as Topic, Internal medicine, Tobacco, Genetics, medicine, Humans, 1112 Oncology and Carcinogenesis, Oncology & Carcinogenesis, Polymorphism, Triglycerides, Genetic association, Genetic risk, Science & Technology, Tobacco Smoke and Health, Prevention, Other Research Radboud Institute for Health Sciences [Radboudumc 0], Human Genome, Case-control study, Odds ratio, medicine.disease, Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], 030104 developmental biology, Case-Control Studies, Body mass index, Genome-Wide Association Study
Abstract

Epidemiologically related traits may share genetic risk factors, and pleiotropic analysis could identify individual loci associated with these traits. Because of their shared epidemiological associations, we conducted pleiotropic analysis of genome-wide association studies of lung cancer (12 160 lung cancer case patients and 16 838 control subjects) and cardiovascular disease risk factors (blood lipids from 188 577 subjects, type 2 diabetes from 148 821 subjects, body mass index from 123 865 subjects, and smoking phenotypes from 74 053 subjects). We found that 6p22.1 (rs6904596, ZNF184) was associated with both lung cancer (P = 5.50x10-6) and blood triglycerides (P = 1.39x10-5). We replicated the association in 6097 lung cancer case patients and 204 657 control subjects (P = 2.40 × 10-4) and in 71 113 subjects with triglycerides data (P = .01). rs6904596 reached genome-wide significance in lung cancer meta-analysis (odds ratio = 1.15, 95% confidence interval = 1.10 to 1.21,Pcombined = 5.20x10-9). The large sample size provided by the lipid GWAS data and the shared genetic risk factors between the two traits contributed to the uncovering of a hitherto unidentified genetic locus for lung cancer. This work was supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD. Transdisciplinary Research for Cancer of Lung (TRICL): National Institute of Health U19 CA148127-01 (PI: Amos), Canadian Cancer Society Research Institute (No. 020214, PI: Hung). The Environment and Genetics in Lung Cancer Etiology (EAGLE), Prostate, Lung, Colon, Ovary Screening Trial (PLCO), and Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) studies were supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute (NCI), Division of Cancer Epidemiology and Genetics. ATBC was also supported by US Public Health Service contracts (N01-CN-45165, N01-RC-45035, and N01-RC-37004) from the NCI. PLCO was also supported by individual contracts from the NCI to the University of Colorado Denver (NO1-CN-25514), Georgetown University (NO1-CN-25522), the Pacific Health Research Institute (NO1-CN-25515), the Henry Ford Health System (NO1-CN-25512), the University of Minnesota (NO1-CN-25513), Washington University (NO1-CN-25516), the University of Pittsburgh (NO1-CN-25511), the University of Utah (NO1-CN-25524), the Marshfield Clinic Research Foundation (NO1-CN-25518), the University of Alabama at Birmingham (NO1-CN-75022), Westat, Inc. (NO1-CN-25476), and the University of California, Los Angeles (NO1-CN-25404). The Cancer Prevention Study-II (CPS-II) Nutrition Cohort was supported by the American Cancer Society. Funding for the Lung Cancer and Smoking study was provided by the National Institutes of Health (NIH), Genes, Environment and Health Initiative (GEI) Z01 CP 010200, NIH U01 HG004446, and NIH GEI U01 HG 004438. For the lung study, the GENEVA Coordinating Center provided assistance with genotype cleaning and general study coordination, and the Johns Hopkins University Center for Inherited Disease Research conducted genotyping. Harvard Lung Study: The Harvard Lung Cancer Study is supported by the National Institutes of Health (R01 CA092824, P50 CA090578, and R01 CA074386). Lung eQTL study: The lung eQTL study at Laval University was supported by the Chaire de pneumologie de la Fondation JD Bégin de l’Université Laval, the Fondation de l’Institut universitaire de cardiologie et de pneumologie de Québec, the Respiratory Health Network of the FRQS, the Canadian Institutes of Health Research (MOP - 123369), and the Cancer Research Society and Read for the Cure. Y. Bossé is the recipient of a Junior 2 Research Scholar award from the Fonds de recherche Québec – Santé (FRQS). Lung meQTL study: The meQTL study based on the environment and Genetics in Lung Cancer Etiology (EAGLE) study was supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services. Epigenetics: This study was supported by NIH grant 1 R01 HL114094 to IAL-O and ZB, NIH grants 1 P30 H101258 and R37HL062569-13 to ZB. ZB is supported by the Ralph Edgington Chair in Medicine. CNM was supported in part by the department of Surgery, University of Southern California. Generation of epigenetic data was supported in part by a Norris Comprehensive Cancer Center core grant, award number P30CA014089, from the National Cancer Institute.

Published
2016
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