TY - JOUR
T1 - International lung cancer consortium
T2 - Coordinated association study of 10 potential lung cancer susceptibility variants
AU - Truong, Therese
AU - Sauter, Wiebke
AU - McKay, James D.
AU - Hosgood, H. Dean
AU - Gallagher, Carla
AU - Amos, Christopher I.
AU - Spitz, Margaret
AU - Muscat, Joshua
AU - Lazarus, Philip
AU - Illig, Thomas
AU - Wichmann, H. Erich
AU - Bickeböller, Heike
AU - Risch, Angela
AU - Dienemann, Hendrik
AU - Zhang, Zuo Feng
AU - Naeim, Behnaz Pezeshki
AU - Yang, Ping
AU - Zienolddiny, Shanbeh
AU - Haugen, Aage
AU - Marchand, Loïc Le
AU - Hong, Yun Chul
AU - Kim, Jin Hee
AU - Duell, Eric J.
AU - Andrew, Angeline S.
AU - Kiyohara, Chikako
AU - Shen, Hongbing
AU - Matsuo, Keitaro
AU - Suzuki, Takeshi
AU - Seow, Adeline
AU - Ng, Daniel P.K.
AU - Lan, Qing
AU - Zaridze, David
AU - Szeszenia-Dabrowska, Neonilia
AU - Lissowska, Jolanta
AU - Rudnai, Peter
AU - Fabianova, Eleonora
AU - Constantinescu, Vali
AU - Bencko, Vladimir
AU - Foretova, Lenka
AU - Janout, Vladimir
AU - Caporaso, Neil E.
AU - Albanes, Demetrius
AU - Thun, Michael
AU - Landi, Maria Teresa
AU - Trubicka, Joanna
AU - Lener, Marcin
AU - Lubinski, Jan
AU - Wang, Ying
AU - Chabrier, Amélie
AU - Boffetta, Paolo
AU - Brennan, Paul
AU - Hung, Rayjean J.
N1 - Funding Information:
US National Institutes of Health, National Cancer Institute (R03 CA133939-01); Central Europe study—World Cancer Research Fund and European Commission’s INCO-COPERNICUS Program (IC15-CT98-0332); Norvegian study—The Norwegian Research Council; Norwegian Cancer Society; Aichi Cancer Center study—-Grants-in-Aid for Scientific Research, Ministry of Education, Science, Sports, Culture and Technology of Japan; MD Anderson study—National Institutes of Health (CA127219, CA55769, CA121197); Penn State study—Public Health Service grants (K99 CA131477), National Institutes of Health (P01 CA68384, K07 CA104231); NCI-China study—Intramural National Cancer Institute program (N01 CO12400); Singapore study—Singapore National Medical Research Council; Seoul study—Eco-technopia 21 project, Ministry of Environment, Republic of Korea; ‘‘Deutsche Krebshilfe’’ (70-2387, 70-2919); Mayo Clinic study—National Institutes of Health (CA77118, CA80127, CA84354); Norris Cotton Cancer Center study—National Center for Research Resources, National Institutes of Health (P20RR018787). Environment and Genetics in Lung Cancer Etiology, Prostate, Lung, Colon, Ovary Screening Trial, Alpha-Tocopherol, Beta-Carotene Cancer Prevention studies, genotyping of Alpha-Tocopherol, Beta-Carotene Cancer Prevention study, Cancer Prevention Study II Nutrition Cohort and part of Prostate, Lung, Colon, Ovary Screening Trial—Intramural Research Program, National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics; Alpha-Tocopherol, Beta-Carotene Cancer Prevention study—US Public Health Service contracts, National Cancer Institute (N01-CN-45165, N01-RC-45035, N01-RC-37004); PLCO study was also supported by individual contracts from the National Cancer Institute to the University of Colorado Denver (NO1-CN-25514); Georgetown University (NO1-CN-25522); Pacific Health Research Institute (NO1-CN-25515); Henry Ford Health System (NO1-CN-25512); University of Minnesota (NO1-CN-25513); Washington University (NO1-CN-25516); University of Pittsburgh (NO1-CN-25511); University of Utah (NO1-CN-25524); Marshfield Clinic Research Foundation (NO1-CN-25518); University of Alabama at Birmingham (NO1-CN-75022); Westat (NO1-CN-25476); University of California, Los Angeles (NO1-CN-25404); The Cancer Prevention Study II Nutrition Cohort was supported by the American Cancer Society; The NIH Genes, Environment and Health Initiative partly funded DNA extraction and statistical analyses (HG-06-033-NCI-01, RO1HL091172-01); genotyping at the Johns Hopkins University Center for Inherited Disease Research (U01HG004438, NIH HHSN268200782096C); study coordination at the GENEVA Coordination Center (U01 HG004446) for Environment and Genetics in Lung Cancer Etiology and part of PLCO studies. German study—BMBF, Germany (Competence Network Radiation Research, project: individual susceptibility and genomic instability); KORA research platform—the Helmholtz Center Munich, German Research Center for Environmental Health.
PY - 2010/1/27
Y1 - 2010/1/27
N2 - 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.
AB - 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.
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U2 - 10.1093/carcin/bgq001
DO - 10.1093/carcin/bgq001
M3 - Article
C2 - 20106900
AN - SCOPUS:77950890482
SN - 0143-3334
VL - 31
SP - 625
EP - 633
JO - Carcinogenesis
JF - Carcinogenesis
IS - 4
ER -
