MDM2 SNP309 rs2279744 polymorphism and gastric cancer risk: a meta-analysis

PLoS One. 2013;8(2):e56918. doi: 10.1371/journal.pone.0056918. Epub 2013 Feb 25.

Abstract

Background: MDM2 is a major negative regulator of p53, and a single nucleotide polymorphism (SNP) in the MDM2 promoter region SNP309 has been demonstrated to be associated with an increased MDM2 expression and a significantly earlier age of onset of several tumors, including gastric cancer. Several studies were published to evaluate the association between SNP309 and gastric cancer risk. However, the results remain conflicting rather than conclusive.

Objective: The aim of this study was to assess the association between the MDM2 SNP309 polymorphism and gastric risk.

Methods: We performed a meta-analysis to investigate this relationship. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the association. The pooled ORs were performed for codominant model, dominant model, and recessive model, respectively.

Results: Five published case-control studies, including 1,621 gastric cancer cases and 2,639 controls were identified. We found that the MDM2 SNP309 polymorphism was associated with a significantly increased risk of gastric cancer risk when all studies were pooled into the meta-analysis (GG versus TT, OR = 1.54; 95%CI = 1.04-2.29, and GG versus GT/TT, OR = 1.49, 95%CI = 1.30-1.72). Furthermore, Egger's test did not show any evidence of publication bias (P = 0.799 for GG versus TT).

Conclusion: Our results suggest that the MDM2 SNP309 polymorphism may be a low-penetrant risk factor for the development of gastric cancer.

Publication types

  • Meta-Analysis

MeSH terms

  • Case-Control Studies
  • Genetic Predisposition to Disease / genetics
  • Humans
  • Odds Ratio
  • Polymorphism, Single Nucleotide / genetics*
  • Proto-Oncogene Proteins c-mdm2 / genetics*
  • Stomach Neoplasms / genetics*

Substances

  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2

Grants and funding

The authors have no funding or support to report.