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Updated: Jun 3, 2026
Generation of Multicellular Human Primary Endometrial Organoids
Published on: October 4, 2019
Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without
Mohamed Khairy Mehasseb1, Rina Panchal, Anthony Henry Taylor
1Reproductive Sciences Section, Department of Cancer Studies and Molecular Medicine, University of Leicester, and Histopathology Department, Leicester Royal Infirmary, University Hospital of Leicester NHS Trust, Leicester, United Kingdom. mohamed.mehasseb@doctors.net.uk
Objective:
To test the hypothesis that the expression of the different isoforms of the estrogen receptor alpha (ER-α) and beta (ER-β) and the progesterone receptor A (PR-A) and B (PR-B) would be differentially modulated in uteri with adenomyosis compared with controls and that modulation would be related to the menstrual cycle.
Design:
Case control, blinded comparison.
Setting:
University department.
Patient(S):
54 premenopausal women with and 35 without uterine adenomyosis as the sole pathology.
Intervention(S):
Multiple samples studied using immunohistochemistry for estrogen and progesterone receptors.
Main Outcome Measure(S):
Histomorphometric analysis of receptor expression.
Result(S):
The ER-α expression in the adenomyotic endometrium was different from that of the normal endometrium and the foci in the midsecretory phase of the cycle, but expression of ER-α in the inner and outer myometrium was not statistically significantly different. The ER-β expression was statistically significantly elevated in the adenomyotic functionalis gland during the proliferative phase and throughout the myometrium across the entire menstrual cycle. Expression of PR-A was similar to that of PR-B, with reduced expression in the basalis stroma, and inner and outer myometrium in the adenomyotic samples. The pattern of ER-β, PR-A, and PR-B expression was similar in the endometrial basalis and adenomyotic foci.
Conclusion(S):
These data suggest ER-β expression and the lack of PR expression are related to the development and/or progression of adenomyosis and might explain the poor response of adenomyosis-associated menstrual symptoms to progestational agents.
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