Lack of association between CYP17 Mspa1 polymorphism and prostate cancer risk: a meta-analysis of 14494 cases and 15971 controls

Medicina (Kaunas). 2013;49(2):51-5.

Abstract

Background and objective: A T-to-C polymorphism that creates a recognition site for the MspA1 restriction enzyme in the 5' promoter region of CYP17 has been implicated as a risk factor for prostate cancer. To date, many studies have evaluated associations between the CYP17 MspA1 polymorphism and prostate cancer risk; however, the results were controversial. Therefore, the aim of this study was to perform a meta-analysis to investigate the association between the CYP17 MspA1 polymorphism and the risk of prostate cancer.

Material and methods: By searching the Pubmed, Web of Science, ScienceDirect, EBSCO databases, 36 studies including 14 494 cases and 15 971 controls were collected. Odds ratios (ORs) with their 95% confidence intervals (CIs) were used to assess the strength of the association.

Results: The overall results showed no significant association between the CYP17 MspA1 polymorphism and the risk of prostate cancer (OR, 1.07; 95% CI, 0.92-1.25 for A2/A2 vs. A1/A1; OR, 1.02; 95% CI, 0.92-1.12 for A1/A2 vs. A1/A1; OR, 1.07; 95% CI, 0.94-1.22 for A2/A2 vs. A1/A2+A1/A1; OR, 1.03; 95% CI, 0.93-1.14 for A1/A2+A2/A2 vs. A1/A1). In the stratified analysis according to ethnicity, no significant associations were observed in Asian, European, and African populations in all genetic models. In the stratified analysis by the source of controls and inpatients were found to have an increased risk of prostate cancer in all genetic models.

Conclusions: The meta-analysis suggests that the CYP17 MspA1 polymorphism is unlikely to increase the risk of prostate cancer in a wide population.

Publication types

  • Meta-Analysis

MeSH terms

  • Alleles
  • Humans
  • Male
  • Polymorphism, Genetic
  • Polymorphism, Restriction Fragment Length
  • Prostatic Neoplasms / epidemiology*
  • Prostatic Neoplasms / genetics*
  • Risk
  • Steroid 17-alpha-Hydroxylase / genetics*

Substances

  • CYP17A1 protein, human
  • Steroid 17-alpha-Hydroxylase