GSTT1 null genotype contributes to increased risk of gastric cancer in Chinese population: evidence from a meta-analysis

Tumour Biol. 2013 Jun;34(3):1691-7. doi: 10.1007/s13277-013-0706-2. Epub 2013 Mar 20.

Abstract

Previous studies suggested glutathione S-transferase T1 (GSTT1) null genotype might be a candidate genetic polymorphism with a role in the susceptibility to gastric cancer, but studies form Chinese population reported controversial findings. Thus, a meta-analysis was performed to clarify the effect of GSTT1 null genotype on gastric cancer risk in Chinese population. Eligible studies were searched in Medline, Embase, and China National Knowledge Infrastructure databases. Between-study heterogeneity was assessed using the I (2) statistic. Odds ratios (OR) with the corresponding 95 % confidence intervals (95 % CI) were pooled to assess the association. Twenty case-control studies involving a total of 3,204 gastric cancer cases and 5,462 controls were finally included in the meta-analysis. Meta-analysis of all 20 studies showed that GSTT1 null genotype was associated with an elevated risk of gastric cancer in Chinese population (OR=1.26, 95 % CI 1.09-1.46, P OR=0.002). The cumulative meta-analysis showed a trend of a more obvious association between GSTT1 null genotype and risk of gastric cancer in Chinese population as information accumulated gradually. Sensitivity analysis by omitting individual study, in turns, did not materially alter the pooled ORs. This meta-analysis provides a strong evidence for the significant association between GSTT1 null genotype and gastric cancer risk in Chinese population, and GSTT1 null genotype contributes to increased risk of gastric cancer.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • China / epidemiology
  • Genetic Predisposition to Disease*
  • Glutathione Transferase / genetics*
  • Humans
  • Polymorphism, Genetic / genetics*
  • Risk Factors
  • Stomach Neoplasms / epidemiology
  • Stomach Neoplasms / etiology*

Substances

  • glutathione S-transferase T1
  • Glutathione Transferase