Abstract
Purpose: A number of case-control studies have been conducted to investigate the association of glutathione S-transferase (GST) genetic polymorphisms and endometrial carcinoma risk. However, these studies have yielded contradictory results. We therefore performed a meta-analysis to derive a more precise estimation of the association between polymorphisms on GSTM1, GSTT1 and endometrial carcinoma. Methods: Identification of relevant studies was carried out through a search in the following databases Medline, EMbase andChinaNational Knowledge International (CNKI) up to March. 2013. All case-control studies that investigated the association between GS-TM1 and GSTT1 gene polymorphisms and risk of endometrial cancer were included in the study. The pooled odds ratio (OR) was used for analyses of results and the corresponding 95% confidence intervals (CI) were estimated. Result: Six published case-control studies of association between the GSTM1 and GSTT1 polymorphism and endometrial cancer risk covering 3558 subjects were included in the metaanalysis, but the results indicated that the null genotypes of GSTM1 and GSTT1 polymorphisms were not associated with a significantly increased risk of endometrial cancer (for GSTM1: OR = 0.99; 95% CI, 0.86 - 1.4; for GSTT1: OR = 0.96; 95% CI, 0.80 - 1.14, respectively). Conclusion: This meta-analysis suggests that GSTM1 and GSTT1 polymorphism may not be associated with increased risk of endometrial cancer. To validate the association between polymorphism and endometrial cancer, further studies with larger numbers of participants worldwide are needed.
Highlights
Endometrial cancer (EC) is the fourth most common cancer in women in developed countries
All case-control studies that investigated the association between GSTM1 and GSTT1 gene polymorphisms and risk of endometrial cancer were included in the study
Result: Six published case-control studies of association between the GSTM1 and GSTT1 polymorphism and endometrial cancer risk covering 3558 subjects were included in the metaanalysis, but the results indicated that the null genotypes of GSTM1 and GSTT1 polymorphisms were not associated with a significantly increased risk of endometrial cancer
Summary
Endometrial cancer (EC) is the fourth most common cancer (after breast, lung, and colorectal cancer) in women in developed countries. Environmental factors have been associated with endometrial cancer in many studies, and a heritable component may predispose to the development of endometrial cancer [1]. EC has predominantly been considered a genetic disease, characterized by sequential accumulation of genetic alterations [3,4]. Endometrial carcinogenesis is a multi-factorial interaction between environmental triggers and genetic susceptibility. Mutagens in the living environment can create DNA adducts and strand breaks, causing genomic instability. Loss of genomic stability and the resulting gene alterations appear to be a crucial molecular and pathogenic step that occurs early in the endometrial carcinogenesis process. Recent studies have revealed that genetic variants in genes controlling carcinogen metabolism, DNA repair and cell
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