Prospective study of effect modification by Toll-Like Receptor 4 variation on the association between Trichomonas vaginalis serostatus and prostate cancer
Platz, Elizabeth A.
Alderete, John F.
Rider, Jennifer R.
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CitationChen, Yen Ching, Yi Ling Huang, Elizabeth A. Platz, John F. Alderete, Lu Zheng, Jennifer R. Rider, Peter Kraft, Edward Giovannucci, and Siobhan Sutcliffe. 2012. “Prospective Study of Effect Modification by Toll-like Receptor 4 Variation on the Association between Trichomonas Vaginalis Serostatus and Prostate Cancer.” Cancer Causes & Control 24 (1): 175–80. https://doi.org/10.1007/s10552-012-0103-y.
AbstractIn previous studies, we observed a positive association between Trichomonas vaginalis serostatus and risk of prostate cancer, particularly aggressive cancer, which we hypothesized might be due to T. vaginalis-mediated intraprostatic inflammation and cell damage. To explore this hypothesis further, we investigated effect modification by Toll-like receptor 4 (TLR4) variation on this association. We hypothesized that TLR4 variation might serve a marker of the anti-trichomonad immune response because T. vaginalis has been shown to elicit inflammation through this receptor.We previously genotyped the non-synonymous TLR4 single nucleotide polymorphism (SNP), rs4986790, and determined T. vaginalis serostatus for 690 incident prostate cancer cases and 692 controls in a nested case-control study within the Health Professionals Follow-up Study.A non-significant suggestion of effect modification was observed by rs4986790 carrier status on the association between T. vaginalis serostatus and prostate cancer risk (p interaction = 0.07). While no association was observed among men homozygous wildtype for this SNP (odds ratio (OR) = 1.23, 95 % confidence interval (CI): 0.86-1.77), a positive association was observed among variant carriers (OR = 4.16, 95 % CI: 1.32-13.1).Although not statistically significant, TLR4 variation appeared to influence the association between T. vaginalis serostatus and prostate cancer risk consistent with the hypothesis that inflammation plays a role in this association. Larger studies will be necessary to explore this possible effect modification further.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41392015
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