Glutathione S-transferase M1 Null Genotype Meta-analysis on Gastric Cancer Risk
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Background: Glutathione S-transferases (GSTs) have proved to be involved in the detoxifying several carcinogens and may play an important role in carcinogenesis of cancer. Previous studies on the association between Glutathione S-transferase M1 (GSTM1) polymorphism and gastric cancer (GC) risk reported inconclusive results. To get a precise result, we conducted this present meta-analysis through pooling all eligible studies.
Methods: A comprehensive databases of Pubmed, Embase, Web of Science, and the Chinese Biomedical Database (CBM) were searched for case-control studies investigating the association between GSTM1 null genotype and GC risk. Odds ratios (OR) and 95% confidence intervals (95% CI) were used to assess this possible association. A χ2-based Q-test was used to examine the heterogeneity assumption. Begg's and Egger's test were used to examine the potential publication bias. The leave-one-out sensitivity analysis was conducted to determine whether our assumptions or decisions have a major effect on the results of present work. Statistical analyses were performed with the software program STATA 12.0.
Results: A total of 47 eligible case-control studies were identified, including 6,678 cases and 12,912 controls. Our analyses suggested that GSTM1 null genotype was significantly associated with increased risk of GC (OR=1.186, 95% CI=1.057-1.329, Pheterogenetiy=0.000, P=0.004). Significant association was also found in Asians (OR=1.269, 95% CI=1.106-1.455, Pheterogenetiy=0.002, P=0.001). However, GSTM1 null genotype was not contributed to GC risk in Caucasians (OR=1.115, 95% CI=0.937-1.326, Pheterogenetiy=0.000, P=0.222). In the subgroup analysis stratified by sources of controls, significant association was detected in hospital-based studies (OR=1.355, 95% CI=1.179-1.557, Pheterogenetiy=0.001, P=0.000), while there was no significant association detected in population-based studies (OR=1.017, 95% CI=0.862-1.200, Pheterogenetiy=0.000, P=0.840).
Conclusion: This meta-analysis showed the evidence that GSTM1 null genotype contributed to the development of GC.
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