Mol. Hum. Reprod. Advance Access originally published online on November 16, 2005
Molecular Human Reproduction 2005 11(10):729-743; doi:10.1093/molehr/gah206
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Glutathione S-transferases M1/T1 gene polymorphisms and endometriosis: a meta-analysis of genetic association studies
Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA
1 To whom correspondence should be addressed at: Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Road, MS 756, Milwaukee, WI 53226-0509, USA. E-mail: swguo{at}mail.mcw.edu
In view of the controversies surrounding the glutathione S-transferases (GST) M1/T1endometriosis 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 6980% publication probability.
Key words: association/endometriosis/genetic/glutathione S-transferase/GSTM1/GSTT1/meta-analysis/polymorphism
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
C.B. Tempfer, M. Simoni, B. Destenaves, and B.C.J.M. Fauser Functional genetic polymorphisms and female reproductive disorders: Part II--endometriosis Hum. Reprod. Update, January 1, 2009; 15(1): 97 - 118. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. W. Montgomery, D. R. Nyholt, Z. Z. Zhao, S. A. Treloar, J. N. Painter, S. A. Missmer, S. H. Kennedy, and K. T. Zondervan The search for genes contributing to endometriosis risk Hum. Reprod. Update, September 1, 2008; 14(5): 447 - 457. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Gentilini, E. Somigliana, P. Vigano, M. Vignali, M. Busacca, and A. M. Di Blasio The vascular endothelial growth factor +405G>C polymorphism in endometriosis Hum. Reprod., January 1, 2008; 23(1): 211 - 215. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. H. Kim, Y. M. Choi, G. H. Lee, M. A. Hong, K. S. Lee, B. S. Lee, J. G. Kim, and S. Y. Moon Association between susceptibility to advanced stage endometriosis and the genetic polymorphisms of aryl hydrocarbon receptor repressor and glutathione-S-transferase T1 genes Hum. Reprod., July 1, 2007; 22(7): 1866 - 1870. [Abstract] [Full Text] [PDF] |
||||

