Aromatase as a therapeutic target in endometriosis

Serdar E. Bulun*, Khaled M. Zeitoun, Kazuto Takayama, Evan Simpson, Hironobu Sasano

*Corresponding author for this work

Research output: Contribution to journalReview article

46 Scopus citations

Abstract

In contrast to normal endometrium, the expression of aromatase is aberrant in endometriosis and is stimulated by prostaglandin E2 (PGE2). This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis - deficient 17β-hydroxysteroid dehydrogenase (17β-HSD) type 2 expression - impairs the inactivation of estradiol (E2) to estrone (E1). These molecular aberrations collectively favor accumulation of increasing quantities of E2 and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis with an aromatase inhibitor.

Original languageEnglish (US)
Pages (from-to)22-27
Number of pages6
JournalTrends in Endocrinology and Metabolism
Volume11
Issue number1
DOIs
StatePublished - Feb 1 2000

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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