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The uterine wall consists of three histological layers: the perimetrium, myometrium, and endometrium. The outermost perimetrium is a thin, serous membrane connected with the broad ligament on the sides, which helps anchor the uterus in the pelvic cavity. The thickest layer, myometrium, is mainly made up of smooth muscle tissue bundles. Its contractions are vital in facilitating the expulsion of the uterine lining, fetus, and placenta during menstruation and childbirth.
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The ovarian cycle regulates endometrial changes throughout a single menstrual cycle via the coordinated action of gonadotrophin-releasing hormone (GnRH) and gonadotrophins.
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The proliferative phase typically occurs after menstruation and lasts between 6 to 13 days in a standard 28-day cycle. This phase involves the reconstruction of the endometrium, guided by estrogen produced by the developing ovarian follicle.
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Correction: Garrido et al. NGF/TRKA Decrease miR-145-5p Levels in Epithelial Ovarian Cancer Cells. <i>Int. J. Mol. Sci.</i> 2020, <i>21</i>, 7657.

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Updated: Feb 24, 2026

Generation of Multicellular Human Primary Endometrial Organoids
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Endometrium and steroids, a pathologic overview.

Francisca Plaza-Parrochia1, Carmen Romero1, Luis Valladares2

  • 1Department of Obstetrics and Gynecology, School of Medicine, University of Chile, Clinical Hospital, Santos Dumont # 999, Santiago, Chile.

Steroids
|August 23, 2017
PubMed
Summary

Sexual steroid alterations, especially estrogens and progestagens, drive endometrial hyperplasia and cancer by disrupting cell proliferation. Risk factors like obesity and PCOS increase endometrial sensitivity to steroids, promoting early-stage disease development.

Keywords:
AdenocarcinomaCancerEndometriaHyperplasiaSteroids

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Area of Science:

  • Gynecology
  • Endocrinology
  • Oncology

Background:

  • Normal endometrial function relies on regulated cell proliferation and differentiation.
  • Disturbances in these processes are linked to endometrial hyperplasia and adenocarcinoma.
  • Alterations in sexual steroid levels and action are key factors in endometrial pathologies.

Purpose of the Study:

  • To review the role of sexual steroids (estrogens, androgens, progestagens) in endometrial hyperplasia and endometrioid adenocarcinoma.
  • To highlight pathological and pharmacological risk factors contributing to endometrial pathologies.
  • To analyze molecular changes induced by steroid alterations in endometrial cancer development.

Main Methods:

  • Literature review focusing on the etiopathogenesis of endometrial hyperplasia and cancer.
  • Analysis of the molecular mechanisms of steroid action on endometrial cells.
  • Examination of risk factors such as obesity, polycystic ovarian syndrome (PCOS), and hormone replacement therapy (HRT).

Main Results:

  • Estrogens stimulate endometrial cell proliferation, while progestagens inhibit proliferation and promote differentiation.
  • Androgen's role in endometrial pathologies remains unclear due to contradictory data.
  • Increased endometrial sensitivity to steroids, observed in conditions like PCOS, contributes to early-stage disease and progression.

Conclusions:

  • Steroid imbalances are central to the development of endometrial hyperplasia and endometrioid adenocarcinoma.
  • Risk factors like obesity, PCOS, and HRT enhance endometrial sensitivity to steroids, promoting pathological cell proliferation.
  • Targeting steroid pathways may offer therapeutic strategies for preventing and treating endometrial cancer.