| Literature DB >> 24662972 |
Jonine D Figueroa1, Summer S Han1, Montserrat Garcia-Closas2, Dalsu Baris1, Eric J Jacobs3, Manolis Kogevinas, Molly Schwenn4, Nuria Malats5, Alison Johnson6, Mark P Purdue1, Neil Caporaso1, Maria Teresa Landi1, Ludmila Prokunina-Olsson1, Zhaoming Wang7, Amy Hutchinson7, Laurie Burdette7, William Wheeler8, Paolo Vineis9, Afshan Siddiq9, Victoria K Cortessis10, Charles Kooperberg11, Olivier Cussenot12, Simone Benhamou13, Jennifer Prescott14, Stefano Porru15, H Bas Bueno-de-Mesquita16, Dimitrios Trichopoulos, Börje Ljungberg17, Françoise Clavel-Chapelon, Elisabete Weiderpass, Vittorio Krogh18, Miren Dorronsoro19, Ruth Travis20, Anne Tjønneland21, Paul Brenan22, Jenny Chang-Claude23, Elio Riboli9, David Conti10, Manuela Gago-Dominguez24, Mariana C Stern10, Malcolm C Pike25, David Van Den Berg10, Jian-Min Yuan26, Chancellor Hohensee11, Rebecca Rodabough11, Geraldine Cancel-Tassin27, Morgan Roupret27, Eva Comperat27, Constance Chen28, Immaculata De Vivo14, Edward Giovannucci29, David J Hunter30, Peter Kraft31, Sara Lindstrom28, Angela Carta15, Sofia Pavanello32, Cecilia Arici15, Giuseppe Mastrangelo33, Margaret R Karagas34, Alan Schned34, Karla R Armenti34, G M Monawar Hosain34, Chris A Haiman35, Joseph F Fraumeni1, Stephen J Chanock1, Nilanjan Chatterjee1, Nathaniel Rothman1, Debra T Silverman1.
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 × 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 × 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 × 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. Published by Oxford University Press 2014.Entities:
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Year: 2014 PMID： 24662972 PMCID： PMC4123644 DOI： 10.1093/carcin/bgu064
Source DB: PubMed Journal: Carcinogenesis ISSN： 0143-3334 Impact factor: 4.944