• Motofumi Suzuki, Takayuki Kurosaki, Tomio Arai, Motoji Sawabe, Takayuki Hosoi, and Tadaichi Kitamura.
• Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. suzukim-uro@h.u-tokyo.ac.jp
• Int. J. Urol. 2007 Sep 1; 14 (9): 800-4.

AimSince catechol estrogens possess carcinogenetic potential, their detoxification may lead to reduced risk of carcinogenesis. Catechol-O-methyltransferase (COMT) catalyzes the O-methylation of catechol estrogens. The enzymatic activity of COMT has been shown to be governed by a functional single-nucleotide polymorphism represented by a G-to-A transition at codon 158, that results in a valine to methionine substitution; this variant form is associated with an up to 4-fold decrease in enzymatic activity. We attempted to investigate whether the Val158Met polymorphism of COMT was associated with the risk of prostate cancer.MethodsWe analysed genomic DNA samples from 324 sporadic prostate cancer patients; 342 controls who had died from causes unrelated to cancer; and 95 Japanese men who were diagnosed as latent prostate cancer by autopsy. The genotyping method we used was a TaqMan assay.ResultsAge adjusted odds ratios for sporadic prostate cancer susceptibility were 1.047 (95% CI: 0.630-1.741) for the G/A genotype and 0.858 (95% CI: 0.407-1.804) for the A/A genotype, as compared with those for the G/G genotype. There was no significant association between this polymorphism and latent prostate cancer susceptibility either.ConclusionsOur results suggested that the Val158Met polymorphism of COMT was not associated with the risk of sporadic or latent prostate cancer in Japanese men.

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