Lack of an association between two BER gene polymorphisms and breast cancer risk: a meta-analysis

PLoS One. 2012;7(12):e50857. doi: 10.1371/journal.pone.0050857. Epub 2012 Dec 14.

Abstract

Background: The base excision repair (BER) pathway removes DNA damage caused by ionizing radiation, reactive oxidative species and methylating agents. ADPRT and APE1 are two important genes in the BER pathway. Several studies have evaluated the association between polymorphisms in the two BER genes (ADPRT Val762Ala and APE1 Asp148Glu) and breast cancer risk. However, the results are inconsistent.

Methodology/principal findings: In this study, we conducted a meta-analysis to derive a more precise estimation. A total of 8 studies were included in the meta-analysis (6 studies with 2,521 cases and 2,652 controls for ADPRT Val762Ala polymorphism and 5 studies with 2,539 cases and 2,572 controls for APE1 Asp148Glu polymorphism). For ADPRT Val762Ala polymorphism, no obvious associations were found for all genetic models (Val/Ala vs. Val/Val: OR = 0.960, 95% CI = 0.845-1.090; Ala/Ala vs. Val/Val: OR = 0.897, 95% CI = 0.683-1.178; dominant model: OR = 0.953, 95% CI = 0.843-1.077; and recessive model: OR = 1.084, 95% CI = 0.838-1.403). For APE1 Asp148Glu polymorphism, also no obvious associations were found for all genetic models (Asp/Glu vs. Asp/Asp: OR = 0.947, 95% CI = 0.829-1.082; Glu/Glu vs. Asp/Asp: OR = 0.958, 95% CI = 0.813-1.129; dominant model: OR = 0.946, 95% CI = 0.835-1.072; and recessive model: OR = 1.004, 95% CI = 0.873-1.155). In the subgroup analysis by ethnicity or study design, still no obvious associations were found.

Conclusions/significance: This meta-analysis indicates that ADPRT Val762Ala and APE1 Asp148Glu polymorphisms are not associated with increased breast cancer risk.

Publication types

  • Meta-Analysis

MeSH terms

  • Breast Neoplasms / genetics*
  • Case-Control Studies
  • DNA Repair*
  • DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics
  • Female
  • Genetic Predisposition to Disease
  • Genetic Variation
  • Genotype
  • Humans
  • Models, Statistical
  • Odds Ratio
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases / genetics
  • Polymorphism, Genetic*
  • Risk

Substances

  • PARP1 protein, human
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • APEX1 protein, human
  • DNA-(Apurinic or Apyrimidinic Site) Lyase

Grants and funding

The authors have no surpport or funding to report.