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Best Pract Res Clin Obstet Gynaecol. 2016 Jul;34:13-24. doi: 10.1016/j.bpobgyn.2015.11.015. Epub 2015 Nov 25.

Hormones and pathogenesis of uterine fibroids.

Author information

1
Division of Human Reproduction, Department of Obstetrics and Gynecology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Electronic address: fmreis@ufmg.br.
2
Department of Morphology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Laboratory of Translational Endocrinology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
3
Laboratory of Translational Endocrinology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

The role of ovarian steroid hormones in the pathogenesis of uterine fibroids is supported by epidemiological, clinical, and experimental evidence. Estradiol and progesterone induce mature leiomyoma cells to release mitogenic stimuli to adjacent immature cells, thereby providing uterine leiomyoma with undifferentiated cells that are likely to support tumor growth. Progesterone action is required for the complete development and proliferation of leiomyoma cells, while estradiol predominantly increases tissue sensitivity to progesterone by increasing the availability of progesterone receptors (PRs). The selective estrogen receptor modulator (SERM) raloxifene and the selective PR modulators (SPRMs) mifepristone, asoprisnil, and ulipristal acetate have been shown in clinical trials to inhibit fibroid growth. The role of sex steroids is critical for leiomyoma development and maintenance, but a number of autocrine and paracrine messengers are involved in this process; hence, numerous pathways remain to be explored in therapeutic innovations for treating this common disease.

KEYWORDS:

estrogen; pathogenesis; progesterone; uterine leiomyoma

PMID:
26725037
DOI:
10.1016/j.bpobgyn.2015.11.015
[Indexed for MEDLINE]

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