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Hum. Reprod. Advance Access originally published online on March 9, 2006
Human Reproduction 2006 21(6):1498-1502; doi:10.1093/humrep/del033
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

CYP17, CYP1A1 and COMT polymorphisms and the risk of adenomyosis and endometriosis in Taiwanese women

S.H. Juo1,5,7, T.N. Wang2, J.N. Lee6, M.T. Wu3, C.Y. Long8 and E.M. Tsai4,6,9

1 Graduate Institute of Medical Genetics, 2 Faculty of Public Health, 3 Graduate Institute of Occupational Safety and Health, 4 Graduate Institute of Medicine, Kaohsiung Medical University, 5 Department of Clinical Research, 6 Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, 7 Department of Medical Research, Mackay Memorial Hospital and 8 Department of Obstetrics and Gynecology, Kaohsiung Municipal Hsiao-Kang Hospital, Taiwan, Republic of China

9 To whom correspondence should be addressed at: 100 Tz-Yu First Road, Kaohsiung City 807, Taiwan, Republic of China. E-mail: tsaieing{at}yahoo.com

BACKGROUND: The aim of the study was to test whether the COMT, CYP1A1 and CYP17 genes influence the risk of developing adenomyosis and endometriosis. METHODS: We conducted two case–control studies, where the cases (n = 198) had either of the two diseases, and controls (n = 312) were disease-free women. For the COMT gene, we selected the G/A nonsynonymous single-nucleotide polymorphism (SNP) that leads to valine-to-methionine (Val/Met) substitution. For the CYP1A1 gene, we used a functional T/C SNP in the 3'-noncoding region, and we genotyped a T/C functional SNP in the 5' region of the CYP17 gene for the present study. Hardy–Weinberg equilibrium was checked in both cases and controls. Logistic regression models were used to evaluate the genetic effect, with adjustment for other covariates. RESULTS: We found that the homozygous COMT genotype that encodes low enzyme activity had an increased risk for adenomyosis with an age-adjusted odds ratio of 3.2 (95% confidence interval 1.3–7.8; P = 0.006). The COMT gene, however, was not associated with endometriosis. Neither the CYP1A1 nor CYP17 genes had any significant association with either of the two diseases. CONCLUSION: The COMT gene significantly influences the risk of adenomyosis but not endometriosis. The present study does not provide evidence to support any of the three genes exerting pleiotropic effects on both diseases.

Key words: adenomyosis/endometriosis/estrogen/gene/polymorphism


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