RNASEL gene polymorphisms and the risk of prostate cancer: a meta-analysis

Clin Cancer Res. 2006 Oct 1;12(19):5713-9. doi: 10.1158/1078-0432.CCR-05-2799.

Abstract

Purpose: Studies revealing conflicting results on the role of RNASEL polymorphisms Glu265X, Arg462Gln, and Asp541Glu on prostate cancer risk led us to perform a meta-analysis to investigate the association of these polymorphisms and prostate cancer risk.

Experimental design: Relevant studies were selected by searching PubMed from January 1996 to August 2005 using keywords "RNASEL gene AND prostate cancer." For each study, odds ratio (OR) with 95% confidence interval (95% CI) was calculated to estimate the gene effect. Pooled estimates of the OR were computed using the random effects model.

Results: Ten studies were included in the meta-analysis. The overall results suggested no major influence of these variants on prostate cancer risk. However, analysis of the Asp541Glu polymorphism by ethnic populations showed that Asp/Glu (familial cases versus control: OR, 1.38; 95% CI, 1.04-1.82; sporadic cases versus control: OR, 1.26; 95% CI, 1.07-1.48; prostate cancer versus control: OR, 1.29; 95% CI, 1.12-1.48) and Asp/Glu + Glu/Glu (familial cases versus control: OR, 1.37; 95% CI, 1.10-1.70; sporadic cases versus control: OR, 1.24; 95% CI, 1.07-1.44; prostate cancer versus control: OR, 1.27; 95% CI, 1.13-1.44) increased prostate cancer risk in Caucasians, thus suggesting a dominant model for the Glu variant.

Conclusions: Compared with the genotype Asp/Asp, the Glu variant at the Asp541Glu polymorphism increases prostate cancer risk by <2-fold in Caucasians, regardless of family history of the disease. This suggests that genuine genetic effects of this polymorphism may account for only a part of prostate cancer in the Caucasian population.

Publication types

  • Comparative Study
  • Meta-Analysis

MeSH terms

  • Antineoplastic Agents
  • Case-Control Studies
  • Endoribonucleases / genetics*
  • Genetic Predisposition to Disease
  • Humans
  • Male
  • Mutation / genetics*
  • Polymorphism, Genetic*
  • Prostate / enzymology
  • Prostatic Neoplasms / enzymology
  • Prostatic Neoplasms / genetics*
  • Risk Factors

Substances

  • Antineoplastic Agents
  • Endoribonucleases
  • 2-5A-dependent ribonuclease