Endometriosis Malignant Transformation: Epigenetics as a Probable Mechanism in Ovarian Tumorigenesis

Jiaxing He, Weiqin Chang, Chunyang Feng, Manhua Cui, Tianmin Xu
International journal of genomics · 2018 · vol. 2018 , pp. 1–13 · doi:10.1155/2018/1465348 · PMID:29780815 · PMC5892233 · W2795326042
review OA: gold CC0 ⤵ 20 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review summarizes epigenetic modifications like DNA methylation, histone changes, and miRNA alterations that likely contribute to malignant transformation in endometriosis and ovarian cancer.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis, defined as the presence of ectopic endometrial glands and stroma outside the uterine cavity, is a chronic, hormone-dependent gynecologic disease affecting millions of women across the world, with symptoms including chronic pelvic pain, dysmenorrhea, dyspareunia, dysuria, and subfertility. In addition, there is well-established evidence that, although endometriosis is considered benign, it is associated with an increased risk of malignant transformation, with the involvement of various mechanisms of development. More and more evidence reveals an important contribution of epigenetic modification not only in endometriosis but also in mechanisms of endometriosis malignant transformation, including DNA methylation and demethylation, histone modifications, and miRNA aberrant expressions. In this present review, we mainly summarize the research progress about the current knowledge regarding the epigenetic modifications of the relations between endometriosis malignant transformation and ovarian cancer in an effort to identify some risk factors probably associated with ectopic endometrium transformation.

My notes (saved in your browser only)

Condition tags

endometriosischronic_pelvic_paindysmenorrheadyspareunia

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 (20)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:19:49.066213+00:00
License: CC0 · commercial use OK