Email updates

Keep up to date with the latest news and content from Diagnostic Pathology and BioMed Central.

Open Access Research

Glutathione S-transferase M1 null genotype meta-analysis on gastric cancer risk

Xianhong Meng1, Yong Liu1* and Bona Liu2

Author Affiliations

1 Department of Gastroenterology, Affiliated to the Fourth Hospital of Harbin Medical University, Harbin 150001, China

2 Department of Oncology, People’s Liberation Army No.202 Hospital, Shenyang 110000, China

For all author emails, please log on.

Diagnostic Pathology 2014, 9:122  doi:10.1186/1746-1596-9-122

Published: 19 June 2014

Abstract

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.

Virtual Slides

The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1644180505119533 webcite.

Keywords:
GSTM1; Polymorphism; Gastric cancer; Risk; Meta-analysis