Association between glutathione S-transferase M1/T1 gene polymorphisms and susceptibility to endometriosis: A systematic review and meta-analysis

Endometriosis is a polygenic/multifactorial disease caused by interactions between multiple genes and the environment. Findings from studies evaluating the association between the glutathione S-transferase (GST) M1/T1 null genotype and susceptibility to endometriosis are inconsistent. This meta-anal...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2016-05, Vol.11 (5), p.1633-1646
Main Authors: XIN, XIAOYAN, JIN, ZHISHAN, GU, HUAJIAN, LI, YUANYUE, WU, TINGTING, HUA, TENG, WANG, HONGBO
Format: Article
Language:English
Subjects:
Asian people
Bias
Care and treatment
Development and progression
Dioxins
Endometriosis
Ethnicity
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gene polymorphisms
Genes
Genetic aspects
Genetic polymorphisms
Genotype & phenotype
Glutathione
glutathione S-transferase M1
glutathione S-transferase T1
Health aspects
Meta-analysis
Pathogenesis
Quality
Studies
White people
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Summary:Endometriosis is a polygenic/multifactorial disease caused by interactions between multiple genes and the environment. Findings from studies evaluating the association between the glutathione S-transferase (GST) M1/T1 null genotype and susceptibility to endometriosis are inconsistent. This meta-analysis updated and reevaluated the possible associations between GSTM1, GSTT1 and combined GSTM1/GSTT1 (null genotype versus wild-type) gene polymorphisms and susceptibility to endometriosis. The PubMed, Embase and Chinese BioMedical Literature databases and Google Scholar were searched for case-control genetic association studies on GSTM1/GSTT1 (null genotype versus wild-type) gene polymorphisms and endometriosis in comparison with non-endometriosis or healthy controls. Fixed-effect and random-effect meta-analytical techniques were conducted for the outcome measure and subgroup analyses. The meta-analysis demonstrated significant associations between the GSTM1 [odds ratio (OR)=1.56; 95% confidence interval (CI): 1.25-1.95; P
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2016.3110