No association between SOD2 Val16Ala polymorphism and breast cancer susceptibility: a meta-analysis based on 9,710 cases and 11,041 controls

Breast Cancer Res Treat. 2010 Jul;122(2):509-14. doi: 10.1007/s10549-009-0725-2. Epub 2010 Jan 6.

Abstract

Breast cancer is the most common cancer in women worldwide, but its etiology is still unclear. It is believed that oxidative stress plays an essential role in the development of breast cancer, while SOD2 is one of the primary enzymes that directly convert potential harmful oxidizing species to harmless metabolites. The association of SOD2 Val16Ala polymorphism and breast cancer risk has been widely reported, but results of previous studies were somewhat contradictory and underpowered. To overcome the limitations of individual study and to understand the real situation, we conducted a systematic review and meta-analysis toward the association between SOD2 Val16Ala polymorphism and breast cancer. Through retrieving MEDLINE, PubMed, Embase, and Web of Science, a total of 17 studies with 9,710 cases and 11,041 controls were identified. The results showed that no significant associations were found for the allele contrast (allele Ala vs. allele Val: OR = 1.020, 95% CI = 0.979-1.062), additive genetic model (Ala/Ala vs. Val/Val: OR = 1.091, 95% CI = 0.969-1.229), dominant genetic model (Ala/Ala +Ala/Val vs. Val/Val: OR = 1.045, 95% CI = 0.961-1.136), and recessive genetic model (Ala/Ala vs. Val/Val +Ala/Val: OR = 1.027, 95% CI = 0.956-1.102). In the stratified analysis by ethnicity and menopausal status, significant associations were also not detected in all genetic models. Conclusively, this meta-analysis strongly suggests that SOD2 Val16Ala polymorphism is not associated with breast cancer susceptibility.

Publication types

  • Meta-Analysis
  • Review
  • Systematic Review

MeSH terms

  • Breast Neoplasms / enzymology
  • Breast Neoplasms / genetics*
  • Case-Control Studies
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Humans
  • Odds Ratio
  • Phenotype
  • Polymorphism, Genetic*
  • Risk Assessment
  • Risk Factors
  • Superoxide Dismutase / genetics*

Substances

  • Superoxide Dismutase
  • superoxide dismutase 2