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Genome-wide interaction study of smoking and bladder cancer risk.


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.

SUBMITTER: Figueroa JD 

PROVIDER: S-EPMC4123644 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Genome-wide interaction study of smoking and bladder cancer risk.

Figueroa Jonine D JD   Han Summer S SS   Garcia-Closas Montserrat M   Baris Dalsu D   Jacobs Eric J EJ   Kogevinas Manolis M   Schwenn Molly M   Malats Nuria N   Johnson Alison A   Purdue Mark P MP   Caporaso Neil N   Landi Maria Teresa MT   Prokunina-Olsson Ludmila L   Wang Zhaoming Z   Hutchinson Amy A   Burdette Laurie L   Wheeler William W   Vineis Paolo P   Siddiq Afshan A   Cortessis Victoria K VK   Kooperberg Charles C   Cussenot Olivier O   Benhamou Simone S   Prescott Jennifer J   Porru Stefano S   Bueno-de-Mesquita H Bas HB   Trichopoulos Dimitrios D   Ljungberg Börje B   Clavel-Chapelon Françoise F   Weiderpass Elisabete E   Krogh Vittorio V   Dorronsoro Miren M   Travis Ruth R   Tjønneland Anne A   Brenan Paul P   Chang-Claude Jenny J   Riboli Elio E   Conti David D   Gago-Dominguez Manuela M   Stern Mariana C MC   Pike Malcolm C MC   Van Den Berg David D   Yuan Jian-Min JM   Hohensee Chancellor C   Rodabough Rebecca R   Cancel-Tassin Geraldine G   Roupret Morgan M   Comperat Eva E   Chen Constance C   De Vivo Immaculata I   Giovannucci Edward E   Hunter David J DJ   Kraft Peter P   Lindstrom Sara S   Carta Angela A   Pavanello Sofia S   Arici Cecilia C   Mastrangelo Giuseppe G   Karagas Margaret R MR   Schned Alan A   Armenti Karla R KR   Hosain G M Monawar GM   Haiman Chris A CA   Fraumeni Joseph F JF   Chanock Stephen J SJ   Chatterjee Nilanjan N   Rothman Nathaniel N   Silverman Debra T DT  

Carcinogenesis 20140324 8


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(-  ...[more]

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