Genome-wide interaction study of smoking and bladder cancer risk
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Figueroa, Jonine
Han, Summer
Garcia-Closas, Montserrat
Baris, Dalsu
Jacobs, Eric
Kogevinas, Manolis
Schwenn, Molly
Malats, Nuria
Johnson, Alison
Purdue, Mark
Caporaso, Neil
Landi, Maria Teresa
Prokunina-Olsson, Ludmila
Wang, Zhaoming
Hutchinson, Amy
Burdette, Laurie
Wheeler, William
Vineis, Paolo
Siddiq, Afshan
Cortessis, Victoria
Kooperberg, Charles
Cussenot, Olivier
Benhamou, Simone
Prescott, Jennifer
Porru, Stefano
Bueno-de-Mesquita, H. Bas
Trichopoulos, Dimitrios
Börje Ljungberg
Françoise Clavel-Chapelon
Weiderpass, Elisabete
Krogh, Vittorio
Dorronsoro, Miren
Travis, Ruth
Tjønneland, Anne
Brenan, Paul
Chang-Claude, Jenny
Riboli, Elio
Conti, David
Gago-Dominguez, Manuela
Stern, Mariana
Pike, Malcolm
Van Den Berg, David
Yuan, Jian-Min
Hohensee, Chancellor
Rodabough, Rebecca
Cancel-Tassin, Geraldine
Roupret, Morgan
Comperat, Eva
Chen, Constance
De Vivo, Immaculata
Giovannucci, Edward
Hunter, David
Kraft, Peter
Lindstrom, Sara
Carta, Angela
Pavanello, Sofia
Arici, Cecilia
Mastrangelo, Giuseppe
Karagas, Margaret
Schned, Alan
Armenti, Karla
Hosain, G. M. Monawar
Haiman, Chris
Fraumeni, Joseph
Chanock, Stephen
Chatterjee, Nilanjan
Rothman, Nathaniel
Silverman, Debra
Published Version
https://doi.org/10.1093/carcin/bgu064Metadata
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Figueroa, J. D., S. S. Han, M. Garcia-Closas, D. Baris, E. J. Jacobs, M. Kogevinas, M. Schwenn, et al. 2014. “Genome-Wide Interaction Study of Smoking and Bladder Cancer Risk.” Carcinogenesis 35 (8): 1737–44. https://doi.org/10.1093/carcin/bgu064.Abstract
Bladder cancer is a complex disease with known environmental and genetic risk factors. We performed a genome-wide interaction study (GWAS) of smoking and bladder cancer risk based on primary scan data from 3002 cases and 4411 controls from the National Cancer Institute Bladder Cancer GWAS. Alternative methods were used to evaluate both additive and multiplicative interactions between individual single nucleotide polymorphisms (SNPs) and smoking exposure. SNPs with interaction P values < 5 x 10(-5) were evaluated further in an independent dataset of 2422 bladder cancer cases and 5751 controls. We identified 10 SNPs that showed association in a consistent manner with the initial dataset and in the combined dataset, providing evidence of interaction with tobacco use. Further, two of these novel SNPs showed strong evidence of association with bladder cancer in tobacco use subgroups that approached genome-wide significance. Specifically, rs1711973 (FOXF2) on 6p25.3 was a susceptibility SNP for never smokers [combined odds ratio (OR) = 1.34, 95% confidence interval (CI) = 1.20-1.50, P value = 5.18 x 10(-7)]; and rs12216499 (RSPH3-TAGAP-EZR) on 6q25.3 was a susceptibility SNP for ever smokers (combined OR = 0.75, 95% CI = 0.67-0.84, P value = 6.35 x 10-7). In our analysis of smoking and bladder cancer, the tests for multiplicative interaction seemed to more commonly identify susceptibility loci with associations in never smokers, whereas the additive interaction analysis identified more loci with associations among smokers-including the known smoking and NAT2 acetylation interaction. Our findings provide additional evidence of gene-environment interactions for tobacco and bladder cancer.Citable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:41392171
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