Molecular Basis of Endometriosis and Endometrial Cancer: Current Knowledge and Future Perspectives

review OA: gold CC0 ⤵ 24 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-08

This review summarizes current molecular knowledge of endometriosis pathophysiology and its potential role in endometrial cancer development, highlighting areas for future research.

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Abstract

The human endometrium is a unique tissue undergoing important changes through the menstrual cycle. Under the exposure of different risk factors in a woman's lifetime, normal endometrial tissue can give rise to multiple pathologic conditions, including endometriosis and endometrial cancer. Etiology and pathophysiologic changes behind such conditions remain largely unclear. This review summarizes the current knowledge of the pathophysiology of endometriosis and its potential role in the development of endometrial cancer from a molecular perspective. A better understanding of the molecular basis of endometriosis and its role in the development of endometrial pathology will improve the approach to clinical management.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometrial Neoplasms Endometriosis Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometriosis Endometriosis Endometriosis Endometriosis Female Genetic Association Studies Humans Ovarian Neoplasms Sequence Analysis, DNA

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (24)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:24:20.309598+00:00
License: CC0 · commercial use OK