V89L polymorphism of the 5alpha-reductase Type II gene (SRD5A2), endogenous sex hormones, and prostate cancer risk

Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):286-91. doi: 10.1158/1055-9965.EPI-07-0238.

Abstract

We examined the combined effect of circulating sex hormones and SRD5A2 V89L polymorphism on prostate cancer risk in a case-control study (300 cases and 300 controls) nested within the Carotene and Retinol Efficacy Trial. A moderate increase in risk associated with above-median serum levels of androstenedione and dehydroepiandrosterone sulfate (DHEAS) was present irrespective of V89L genotype. However, in L/L or V/L men, above-median DHEAS levels were associated with an increased risk of aggressive tumors [odds ratios (OR), 3.12; 95% confidence interval (95% CI), 1.28-7.63] but not of nonaggressive ones (OR, 0.56; 95% CI, 0.25-1.25). Above-median serum levels of free estradiol were associated with a lower risk, especially for aggressive cancer. The association with aggressive disease was more pronounced in men with a V/V genotype (OR, 0.34; 95% CI, 0.14-0.81), than in men with an L/L or V/L genotype (OR, 0.77; 95% CI, 0.37-1.60). Above-median levels of 3alpha-diol G were associated with an increased risk, but only in men with the L/L or V/L genotype (OR, 2.16; 95% CI, 1.31-3.56). The increase in risk in L/L and V/L men was restricted to aggressive tumors. Our study observed that only in men with the L/L or V/L genotype were increased serum levels of DHEAS and 3alpha-diol G positively associated with a higher risk of aggressive prostate cancer. Free estradiol levels were negatively associated with risk of aggressive prostate cancer in men with the V/V genotype. However, the absence of an overall association between V89L genotype and aggressive prostate cancer argues for a cautious interpretation of these observations.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / genetics*
  • Aged
  • Case-Control Studies
  • Genotype
  • Gonadal Steroid Hormones / blood*
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Polymorphism, Genetic*
  • Prostatic Neoplasms / blood*
  • Prostatic Neoplasms / genetics*
  • Risk Factors

Substances

  • Gonadal Steroid Hormones
  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase