Hormones and pathogenesis of uterine fibroids

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 wit...

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Published inBest practice & research. Clinical obstetrics & gynaecology Vol. 34; pp. 13 - 24
Main Authors Reis, Fernando M., MD, PhD, Bloise, Enrrico, DVM, PhD, Ortiga-Carvalho, Tânia M., PhD
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.07.2016
Subjects
Animals
Cell Transformation, Neoplastic - drug effects
Contraceptives, Oral, Hormonal
Estradiol - metabolism
Estradiol - pharmacology
estrogen
Extracellular Matrix - drug effects
Extracellular Matrix - secretion
Female
Humans
Leiomyoma - drug therapy
Leiomyoma - etiology
Leiomyoma - metabolism
Leiomyoma - pathology
Obstetrics and Gynecology
pathogenesis
progesterone
Progesterone - metabolism
Progesterone - pharmacology
Progestins - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Selective Estrogen Receptor Modulators - therapeutic use
Signal Transduction
uterine leiomyoma
Uterine Neoplasms - drug therapy
Uterine Neoplasms - etiology
Uterine Neoplasms - metabolism
Uterine Neoplasms - pathology
pathogenesis
estrogen
uterine leiomyoma
progesterone
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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.
AbstractList 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. •Both estradiol and progesterone are essential for uterine fibroid development.•Ovarian blockade arrests leiomyoma growth, but it has many side effects.•Autocrine and paracrine factors are induced by sex steroids in fibroid cells.•Leiomyomas may be more responsive to sex steroids than normal myometrium.•Future research should map specific pathways of hormone action in fibroids.
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.
Author Bloise, Enrrico, DVM, PhD
Ortiga-Carvalho, Tânia M., PhD
Reis, Fernando M., MD, PhD
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Keywords pathogenesis
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Snippet The role of ovarian steroid hormones in the pathogenesis of uterine fibroids is supported by epidemiological, clinical, and experimental evidence. Estradiol...
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SubjectTerms Animals
Cell Transformation, Neoplastic - drug effects
Contraceptives, Oral, Hormonal
Estradiol - metabolism
Estradiol - pharmacology
estrogen
Extracellular Matrix - drug effects
Extracellular Matrix - secretion
Female
Humans
Leiomyoma - drug therapy
Leiomyoma - etiology
Leiomyoma - metabolism
Leiomyoma - pathology
Obstetrics and Gynecology
pathogenesis
progesterone
Progesterone - metabolism
Progesterone - pharmacology
Progestins - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Selective Estrogen Receptor Modulators - therapeutic use
Signal Transduction
uterine leiomyoma
Uterine Neoplasms - drug therapy
Uterine Neoplasms - etiology
Uterine Neoplasms - metabolism
Uterine Neoplasms - pathology
Title Hormones and pathogenesis of uterine fibroids
URI https://www.clinicalkey.es/playcontent/1-s2.0-S1521693415002291
https://dx.doi.org/10.1016/j.bpobgyn.2015.11.015
https://www.ncbi.nlm.nih.gov/pubmed/26725037
https://search.proquest.com/docview/1807884333
Volume 34
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