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Submitted on December 19, 2006
Accepted on May 7, 2007
Department of Obstetrics and Gynecology, Stanford University, Stanford, California 94305 (R.O.B., M.N., C.R.N.); Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, California (S.T., A.E.H., K.C.V., L.C.G.); Department of Obstetrics and Gynecology, University Medical Group, Greenville Hospital System, Greenville, South Carolina 29605 (B.A.L.)
* To whom correspondence should be addressed. E-mail: giudice{at}obgyn.ucsf.edu.
The identification of molecular differences in the endometrium of women with endometriosis is an important step toward understanding the pathogenesis of this condition and toward developing novel strategies for the treatment of associated infertility and pain. In this study, we conducted global gene expression analysis of endometrium from women with and without moderate/severe stage endometriosis and compared the gene expression signatures across various phases of the menstrual cycle. The transciptome analysis revealed molecular dysregulation of the proliferative-to-secretory transition in endometrium of women with endometriosis. Paralleled gene expression analysis of endometrial specimens obtained during the early secretory phase demonstrated a signature of enhanced cellular survival and persistent expression of genes involved in DNA synthesis and cellular mitosis in the setting of endometriosis. Comparative gene expression analysis of progesterone-regulated genes in secretory phase endometrium confirmed the observation of attenuated progesterone response. Additionally, interesting candidate susceptibility genes were identified that may be associated with this disorder, including FOXO1A, MIG6, and CYP26A1. Collectively, these findings provide a framework for further investigations on causality and mechanisms underlying attenuated progesterone response in endometrium of women with endometriosis.
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