Glutathione S-transferases M1/T1 gene polymorphisms and endometriosis: a meta-analysis of genetic association studies

Sun-Wei Guo, Sun‐Wei Guo
Molecular human reproduction · 2005 · vol. 11(10) , pp. 729–743 · doi:10.1093/molehr/gah206 · PMID:16291859 · W2108985731
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This meta-analysis of 14 GSTM1 studies and nine GSTT1 studies found no increased endometriosis risk with the GSTM1 null genotype but a potential 29% higher risk with the GSTT1 null genotype, though publication bias was noted.

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Abstract

In view of the controversies surrounding the glutathione S-transferases (GST) M1/T1-endometriosis association, a meta-analysis of the GSTM1/GSTT1 genetic association studies of endometriosis was performed. In this meta-analysis involving 14 GSTM1 studies with 1539 cases and 1805 controls and nine GSTT1 studies with 746 cases and 834 controls, respectively, substantial heterogeneities among studies were found. In addition, asymmetry in funnel plot was evident, which is likely to stem from publication bias, given no apparent indication of true heterogeneity. The bias appears to be prominent for GSTM1 studies, but is less so for GSTT1 studies. After correction for this bias, there is no evidence that women with GSTM1 null genotype have increased risk of developing endometriosis as compared with women with other genotypes. For GSTT1, the risk associated with the null genotype is 29% higher than other genotypes. However, even this estimate should be viewed with a large grain of salt, because the estimate could easily lose its statistical significance if there is a realistic 69-80% publication probability.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Glutathione Transferase Publication Bias Adult Endometriosis Endometriosis Female Genotype Glutathione Transferase Humans Middle Aged Polymorphism, Genetic

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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Cited by (48)

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