Endometriosis Research - Causes, Treatment, Symptoms, Infertility

Endometriosis Research Today is a free monthly online journal that collates and summarizes the latest research about Endometriosis, including details on causes, treatment, symptoms, infertility.


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A selective estrogen receptor-beta agonist causes lesion regression in an experimentally induced model of endometriosis.

Harris HA, Bruner-Tran KL, Zhang X, Osteen KG, Lyttle CR

Women's Health Research Institute, Wyeth Research, Collegeville, PA 19426, USA. harrish@wyeth.com

BACKGROUND: Endometriosis is a common gynaecological problem of uncertain aetiology. It affects primarily young, reproductive-aged women and can result in chronic pelvic pain and infertility. Current approved therapies have significant side-effects and hysterectomy is employed as a final solution. ERB-041 is a selective estrogen receptor-beta (ERbeta) agonist that has anti-inflammatory activity in preclinical models of arthritis and inflammatory bowel disease, but is inactive in many preclinical models of classic estrogen activity. Because endometriosis is now thought to be, at least in part, an inflammatory disease, we evaluated ERB-041's activity in an experimentally induced model of endometriosis. METHODS: Athymic nude mice (ovariectomized or intact) were implanted with tissue fragments of normal human endometrium. After establishment of lesions for 11-14 days, mice were treated with ERB-041 for 15-17 days. Upon euthanasia, the number of lesions, their size and location were noted. Five lesions were recovered for RNA analysis. RESULTS: Across six studies, ERB-041 caused complete lesion regression in 40-75% of the mice studied. The compound appeared to be equally effective in gonad-intact as in ovariectomized mice, and analysed recovered lesions expressed ERalpha but not ERbeta mRNA. CONCLUSIONS: ERB-041 and possibly other ERbeta selective agonists may be a useful new approach to treating endometriosis.

Published 24 March 2005 in Hum Reprod, 20(4): 936-41.
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Endometriosis Research Today Archive:

Volume 1 (2004)
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Volume 2 (2005)
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