Citations 2
Genome-wide interaction analysis identified low-frequency variants with sex disparity in lung cancer risk
Li, Yafang , Xiao, Xiangjun , Byun, Jinyoung , Cheng, Chao , Bossé, Yohan , McKay, James , Lam, Stephen , Tardón, Adonina , Chen, Chu , Landi, Maria Teresa , Wichmann, Erich, Goodman, Gary, Field, John K. , Shete, Sanjay , Melander, Olle , Andrew, Angeline S. , Grankvist, Kjell , Johansson, Mikael , Caporaso, Neil E. , Aldrich, Melinda C. , Schwartz, Ann G. , Gorlov, Ivan P. , Purrington, Kristen S. , Yang, Ping , Bailey‐Wilson, Joan E. , Liu, Yanhong , Mandal, Diptasri , Gaba, Colette , Brennan, Paul , Cheng, Chao , Wilson, Richard K , Field, John K , Tardón, Adonina , Bossé, Yohan , Grankvist, Kjell , Purrington, Kristen S , Byun, Jinyoung , Li, Jianrong , Albanes, Demetrius , Bojesen, Stig E. , Johansson, Mattias , Risch, Angela , Bickeböller, Heike , Christiani, David C. , Rennert, Gad , Arnold, Susanne M. , Marchand, Loı̈c Le , Brunnström, Hans , Liu, Geoffrey , Hung, Rayjean J. , Kiemeney, Lambertus A. , Shen, Hongbing , Sun, Ryan , Zienolddiny, Shanbeh , Teare, M. Dawn , Hong, Yun‐Chul , Davies, Michael P.A. , Lazarus, Philip J. , Schabath, Matthew B. , Han, Younghun , Pinney, Susan M. , Willey, James C. , Amos, Christopher I.
No container title available | July 13, 2021 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract There is growing evidence showing that sex disparity in lung cancer risk cannot be fully explained by sex differences in smoking behavior, implying existence of genetic and molecular basis for sex disparity in lung cancer development. However, the information about sex dimorphism in lung cancer risk is quite limited despite the great success in lung cancer association studies. By adopting a stringent two-stage analysis strategy, we performed a genome-wide gene-sex interaction analysis using genotype from a lung cancer cohort including ~ 47,000 individuals with European ancestry. Three low-frequency variants (minor allele frequency < 0.05), rs17662871 (OR=0.71, p=4.29x10-8); rs79942605 (OR=2.17, p=2.81x10-8); and rs208908 (OR=0.70, p=4.54x10-8), were identified with different risk effect of lung cancer between men and women. Further eQTL and functional annotation analysis suggested rs208908 affect lung cancer risk through differential regulation of CXADR (Coxsackie Virus And Adenovirus Receptor) gene expression in lung tissues between men and women. Our study is one of the first studies to provide novel insights about the genetic and molecular basis for sex disparity in lung cancer development.
Abstract 4826: International Lung Cancer Consortium: Pooled analysis of previous lung diseases and lung cancer risk
Brenner, Darren R. , Bickeböller, Heike , Wichmann, Erich, Schwartz, Ann G. , Friis, Søren, Field, John K. , McLaughlin, John R., Lan, Qing , Park, Bernard J. , Hung, Rayjean J., Boffetta, Paolo , Duell, Eric J. , Rosenberger, Albert , Muscat, Joshua E. , Yang, Ping , Tjønneland, Anne , Marchand, Loı̈c Le , Zhang, Zuo‐Feng , Lazarus, Philip J. , McLaughlin, John R., Wiencke, John K. , Neri, Monica , Orlow, Irene , Hung, Rayjean J., Field, John K , Bickeböller, Heike
Cancer Research | February 25, 2011 | Volume: 70 | Issue: 8_Supplement | Pages: 4826-4826
Abstract To clarify the role of previous lung diseases (PLDs) (chronic bronchitis, emphysema, pneumonia, tuberculosis, asbestosis and silicosis) in the development of lung cancer we conducted a pooled analysis in the International Lung Cancer Consortium (ILCCO). Data from 16 studies (9 population based case-control, 4 hospital based case-control, 2 mixed case-control and 1 cohort - 10 from North America, 5 from Europe and 1 from Asia) were pooled, including 24044 cases and 81256 controls. Study-specific effect estimates were derived using logistic regression models for case-control studies and Cox proportional hazards models for cohort studies adjusted for age, sex, education and pack-years of smoking. Effect estimates were then pooled using random effects models where summary effects for each of the PLDs were evaluated separately. Stratified analyses were conducted based on smoking status, histology and study design or control source. Heterogeneity was evaluated using the Cochrane Q statistic and Galbraith plots, and publication bias was evaluated using funnel plots as well as the Begg test. A previous history of emphysema conferred a relative risk (RR) of 2.17, 95% confidence interval (CI): 1.67-2.82 (from 15 studies, p-het<.001). A previous history of chronic bronchitis conferred a RR of 1.49, 95% CI: 1.33-1.60 (from 12 studies, p-het.=0.434). Tuberculosis was associated with a RR of 1.54, 95% CI: 1.19-1.99 (from 15 studies, p-het.=0.001). Both asbestosis (RR 2.51, 95% CI: 1.53-4.12 (from 7 studies, p-het=0.379)) and silicosis (RR 1.70, 95% CI: 1.15-2.54, (from 3 studies, p-het. p=0.476)) were also associated with lung cancer risk. When the outlying studies were removed, effect estimates changed minimally and heterogeneity was reduced. Findings were consistent in subgroup analyses by smoking status and histology (adenocarcinoma, squamous cell carcinoma and small cell lung cancer). Effect estimates among never smokers were for emphysema a RR of 2.21, 95% CI: 0.99-4.90 (from 8 studies), for chronic bronchitis 1.12, 95% CI: 0.78-1.62 (from 9 studies), for pneumonia 1.37, 95% CI: 1.10-1.70 (from 10 studies) and for tuberculosis 1.54, 95% CI: 0.99-2.39 (from 9 studies). In this analysis of data from multiple continents, PLDs were associated with an increased risk of lung cancer. The evidence among never smokers supports a direct relationship between previous lung diseases and lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4826.