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Review
. 2017 Jun 23:8:47.
doi: 10.4103/ijpvm.IJPVM_346_15. eCollection 2017.

Is There Any Association between Glutathione S-transferases M1 and Glutathione S-transferases T1 Gene Polymorphisms and Endometrial Cancer Risk? A Meta-analysis

Xiuxiu Yin  1 , Jie Chen  2
Affiliations
Review

Is There Any Association between Glutathione S-transferases M1 and Glutathione S-transferases T1 Gene Polymorphisms and Endometrial Cancer Risk? A Meta-analysis

Xiuxiu Yin et al. Int J Prev Med. .

Abstract

Epidemiological evidence on the association between genetic polymorphisms in glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) genes and risk of endometrial cancer (EC) has been inconsistent. In this meta-analysis, we seek to investigate the relationship between GSTM1 and GSTT1 polymorphisms and the risk of EC. We searched Medline, PubMed, Web of Science, Embase, Chinese National Knowledge Infrastructure database, and Chinese Biomedical Literature database to identify eligible studies. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) for the association were determined using a fixed- or random-effect model. Tests for heterogeneity of the results and sensitivity analyses were performed. A total of six case-control studies were included in the final meta-analysis of GSTM1 (1293 cases and 2211 controls) and GSTT1 (1286 cases and 2200 controls) genotypes. Overall, GSTM1 null genotype was not significantly associated with an increased risk of EC (OR = 1.00, 95% CI = 0.76-1.30, P = 0.982). Similarly, for GSTT1 deletion genotype, we observed no association under the investigated model in the overall analysis (OR = 0.91, 95% CI = 0.64-1.30, P = 0.619). Subgroup analysis also showed no significant association between the GSTM1 null genotype and EC risk in hospital-based design (OR = 1.26, 95% CI = 0.93-1.71, P = 0.131) and no relationship between GSTT1 null genotype with EC risk in population-based design (OR = 1.18, 95% CI = 0.79-1.76, P = 0.407). However, GSTM1 null genotype contributed to an increased EC risk in population-based design (OR = 0.76, 95% CI = 0.60-0.97, P = 0.027), while null GSTT1 in hospital-based studies (OR = 0.70, 95% CI = 0.52-0.93, P = 0.015). The present meta-analysis suggested that GSTs genetic polymorphisms may not be involved in the etiology of EC. Large epidemiological studies with the combination of GSTM1 null, GSTT1 null, and design-specific with the development of EC are needed to prove our findings.

Keywords: Endometrial cancer; glutathione S-transferases M1; glutathione S-transferases T1; meta-analysis; susceptibility.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
Flowchart of study selection
Figure 2
Figure 2
(a) Forest plot for the overall association between glutathione S-transferases M1 null genotype and endometrial cancer risk. (b) Forest plot for the overall association between glutathione S-transferases T1 null genotype and endometrial cancer risk
Figure 3
Figure 3
(a) Relationship between glutathione S-transferases M1 null genotype and endometrial cancer risk by study design. (b) Relationship between glutathione S-transferases T1 null genotype and endometrial cancer risk by study design
Figure 4
Figure 4
(a) Funnel plot for glutathione S-transferases M1 gene polymorphism and endometrial cancer risk. (b) Funnel plot for glutathione S-transferases T1 gene polymorphism and endometrial cancer risk
See this image and copyright information in PMC

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