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Microdissection and Dissociation of the Murine Oviduct: Individual Segment Identification and Single Cell Isolation

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Published on: November 4, 2021

Adenomyosis pathogenesis: insights from next-generation sequencing.

Serdar E Bulun¹, Sule Yildiz¹, Mazhar Adli¹

¹Division of Reproductive Science in Medicine, Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.

Human Reproduction Update

|June 16, 2021

Summary

Next-generation sequencing reveals KRAS mutations in endometrial cells are key to adenomyosis development, supporting the invagination theory. These mutations drive disease progression and progesterone resistance, linking adenomyosis to endometriosis pathogenesis.

Keywords:

ESR1 KRAS NGS PGR adenomyosis driver mutation endometriosis endometrium next-generation sequencing progesterone resistance

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Area of Science:

Gynecology
Molecular Biology
Genetics

Background:

Adenomyosis is a complex uterine disorder characterized by endometrial tissue within the myometrium, causing pain, bleeding, and infertility.
Its origins and the roles of endometrial and myometrial cells are not fully understood, with competing invagination and metaplasia theories.
Diagnosis and management remain challenging.

Purpose of the Study:

To investigate the cellular origins of adenomyosis using next-generation sequencing (NGS).
To identify genetic mutations and signaling pathways involved in adenomyosis pathogenesis, survival, and growth.
To compare the molecular characteristics of adenomyosis with endometriosis and uterine fibroids.

Main Methods:

Comprehensive literature search of PubMed for studies on adenomyosis, endometriosis, and related genetic analyses.
Utilized next-generation sequencing (NGS) data, including whole-exome and whole-genome sequencing, RNA sequencing, and targeted deep sequencing.
Focused on identifying driver mutations, epigenetic changes, and gene expression patterns related to steroid hormone action.

Main Results:

Recurring KRAS mutations were identified in epithelial cells of both adenomyosis and adjacent basalis endometrium, supporting the invagination theory.
Identical KRAS mutations were found in adenomyosis, eutopic endometrium, and endometriosis, suggesting a shared origin from mutated endometrial cell populations.
These mutations activate pathways promoting cell survival and proliferation, contributing to progesterone resistance in adenomyosis.

Conclusions:

Adenomyosis likely originates from the entrapment of basalis endometrial glands with KRAS mutations within the myometrium.
KRAS mutations are a common driver mutation in both adenomyosis and endometriosis, indicating similar pathogenic mechanisms.
These genetic alterations contribute to key features of adenomyosis, including prolonged cell survival and progesterone resistance.