Genome-wide interaction study of smoking and bladder cancer risk
26904 bgu064.pdf (592.3Kb)
Access StatusFull text of the requested work is not available in DASH at this time ("dark deposit"). For more information on dark deposits, see our FAQ.
Landi, Maria Teresa
Bueno-de-Mesquita, H. Bas
Van Den Berg, David
De Vivo, Immaculata
Hosain, G. M. Monawar
MetadataShow full item record
CitationFigueroa, 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.
AbstractBladder 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 pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41392171
- SPH Scholarly Articles