Mechanisms of excessive estrogen formation in endometriosis

Serdar E. Bulun; Bilgin Gurates; Zongjuan Fang; Mitsutoshi Tamura; Siby Sebastian; Jianfeng Zhou; Sanober Amin; Sijun Yang

doi:10.1016/S0165-0378(01)00132-2

Mechanisms of excessive estrogen formation in endometriosis

Serdar E. Bulun^*, Bilgin Gurates, Zongjuan Fang, Mitsutoshi Tamura, Siby Sebastian, Jianfeng Zhou, Sanober Amin, Sijun Yang

^*Corresponding author for this work

Obstetrics and Gynecology

Research output: Contribution to journal › Article › peer-review

94 Scopus citations

Abstract

Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE₂. This results in local production of estrogen, which induces PGE₂ formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17β-hydroxysteroid dehydrogenase (17β-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE₂ in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor.

Original language	English (US)
Pages (from-to)	21-33
Number of pages	13
Journal	Journal of Reproductive Immunology
Volume	55
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-0378(01)00132-2
State	Published - 2002

Funding

We thank Margarita Guerrero and Dee Alexander for providing expert editorial assistance. This research work was supported, in part, by the NIH grant HD38691.

Keywords

17β-Hydroxysteroid dehydrogenase type 2
Aromatase
Aromatase inhibitor
Cyclo-oxygenase
Endometriosis
Estrogen
Estrogen biosynthesis
Estrogen metabolism
Osteoporosis
Progesterone
Prostaglandin E
Steroidogenesis

ASJC Scopus subject areas

Obstetrics and Gynecology
Immunology and Allergy
Immunology
Reproductive Medicine

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10.1016/S0165-0378(01)00132-2

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title = "Mechanisms of excessive estrogen formation in endometriosis",

abstract = "Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE2. This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17β-hydroxysteroid dehydrogenase (17β-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor.",

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author = "Bulun, {Serdar E.} and Bilgin Gurates and Zongjuan Fang and Mitsutoshi Tamura and Siby Sebastian and Jianfeng Zhou and Sanober Amin and Sijun Yang",

note = "Funding Information: We thank Margarita Guerrero and Dee Alexander for providing expert editorial assistance. This research work was supported, in part, by the NIH grant HD38691.",

year = "2002",

doi = "10.1016/S0165-0378(01)00132-2",

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AU - Bulun, Serdar E.

AU - Gurates, Bilgin

AU - Fang, Zongjuan

AU - Tamura, Mitsutoshi

AU - Sebastian, Siby

AU - Zhou, Jianfeng

AU - Amin, Sanober

AU - Yang, Sijun

N1 - Funding Information: We thank Margarita Guerrero and Dee Alexander for providing expert editorial assistance. This research work was supported, in part, by the NIH grant HD38691.

PY - 2002

Y1 - 2002

N2 - Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE2. This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17β-hydroxysteroid dehydrogenase (17β-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor.

AB - Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE2. This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17β-hydroxysteroid dehydrogenase (17β-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor.

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KW - Estrogen metabolism

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KW - Prostaglandin E

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Mechanisms of excessive estrogen formation in endometriosis

Abstract

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Keywords

ASJC Scopus subject areas

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