Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis.

Serdar E. Bulun, S E Bulun, Khaled Zeitoun, K Zeitoun, K Takayama, Ken‐ichi Takayama, Leslie R. Noble, L Noble, D Michael, E Simpson, E R Simpson, A Johns, Michael Putman, M Putman, Hironobu Sasano, H Sasano
Endocrine-related cancer · 1999 · vol. 6(2) , pp. 293–301 · doi:10.1677/erc.0.0060293 · PMID:10731122 · W2162403751
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Endometriotic stromal cells express aromatase to produce estrogen locally, which promotes PGE2, a positive feedback inducer of aromatase, and aromatase inhibitors have successfully treated aggressive endometriosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

This paper reviews and synthesizes evidence on estrogen production in endometriosis, focusing on how local steroidogenic pathways in endometriotic stromal cells differ from eutopic endometrium. It describes an autocrine positive feedback loop where aberrant aromatase expression in endometriotic stromal cells increases estrogen synthesis, which then enhances COX-2 and drives high PGE2, and PGE2 further induces aromatase; it also notes that aromatase expression is controlled by opposing transcription factors (SF-1 stimulatory versus COUP-TF inhibitory factors) and that endometriotic tissue shows deficiency of 17β-HSD type 2, reducing estradiol-17β inactivation. A key caveat is that much of the presented basis comes from laboratory/biochemical and cited prior studies rather than a single new controlled clinical experiment across cohorts. This paper is centrally about endometriosis — specifically, local estrogen biosynthesis via aromatase and the use of aromatase inhibitors to treat aggressive recurrent endometriosis.

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Abstract

Estrogen is the most important known factor that stimulates the growth of endometriosis. Estrogen delivery to endometriotic implants was classically viewed to be only via the circulating blood in an endocrine fashion. We recently uncovered an autocrine positive feedback mechanism, which favored the continuous production of estrogen and prostaglandin (PG)E2 in the endometriotic stromal cells. The enzyme, aromatase, is aberrantly expressed in endometriotic stromal cells and catalyzes the conversion of C19 steroids to estrogens, which then stimulate cyclooxygenase-2 to increase the levels of PGE2. PGE2, in turn, is a potent inducer of aromatase activity in endometriotic stromal cells. Aromatase is not expressed in the eutopic endometrium. Aromatase expression in endometriosis and its inhibition in eutopic endometrium are controlled by the competitive binding of a stimulatory transcription factor, steroidogenic factor-1, and an inhibitory factor, chicken ovalbumin upstream promoter-transcription factor to a regulatory element in the aromatase P450 gene promoter. In addition, we find that endometriotic tissue is deficient in 17beta-hydroxysteroid dehydrogenase type 2, which is normally expressed in eutopic endometrial glandular cells and inactivates estradiol-17beta to estrone. This deficiency is another aberration that favors higher levels of estradiol-17beta in endometriotic tissues in comparison with the eutopic endometrium. The clinical relevance of local aromatase expression in endometriosis was exemplified by the successful treatment of an unusually aggressive form of recurrent endometriosis in a postmenopausal woman using an aromatase inhibitor.

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Condition tags

endometriosis

MeSH descriptors

Aromatase Inhibitors Endometriosis Endometriosis Enzyme Inhibitors Estrogens Aromatase Aromatase Endometriosis Endometriosis Enzyme Inhibitors Estrogens Female Humans

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