Integrating modern approaches to pathogenetic concepts of malignant transformation of endometriosis

Hiroshi Kobayashi, Yuki Yamada, Naoki Kawahara, Kenji Ogawa, Chiharu Yoshimoto
Oncology reports · 2018 · vol. 41(3) , pp. 1729–1738 · doi:10.3892/or.2018.6946 · PMID:30592289 · W2905981484
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review synthesizes findings on the shared and distinct genetic pathways, environmental factors like iron, and subtype-specific 'go or stop' mechanisms underlying malignant transformation in endometriosis-associated ovarian cancers.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This paper provides a literature review of mechanisms underlying malignant transformation of endometriosis-associated ovarian cancer (EAOC), focusing on shared and subtype-specific (epi)genetic backgrounds between endometrioid carcinoma (EC) and clear cell carcinoma (CCC). It proposes that both EC and CCC share overlapping molecular signatures and environmental redox stressors from repeated hemorrhage (hemoglobin, heme, and iron), but also exhibit a subtype-dependent “go or stop” pattern where estrogen receptor activity promotes EC proliferation and HNF-1β-mediated cell cycle arrest relates to CCC under oxidative stress. The authors summarize evidence that cyst fluid hemoglobin and iron–related measurements are significantly lower in EAOC than in benign ovarian endometrioma, while also noting assay-related limitations where different measurement methods can yield different iron estimates. This paper is centrally about endometriosis—malignant transformation of endometriosis into EAOC via shared (epi)genetic and redox imbalance concepts, with EC/CCC subtype-specific drivers.

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Abstract

In the present study, we summarize the role of the shared and independent (epi)genetic background between endometrioid carcinoma (EC) and clear cell carcinoma (CCC), two histological subtypes of endometriosis-associated ovarian cancer (EAOC). Using the PubMed database, we conducted a literature review of various studies related to the malignant transformation of endometriosis. Both endometriosis and EAOC face potential environmental hazards, including hemoglobin (Hb), heme and free iron, which induces DNA damage and mutations. Although EC is distinguished from CCC due to different morphologies, both represent common environmental profiles and maintain the similar (epi)genomic abnormalities with multiple overlaps and share similar molecular signatures. By contrast, EAOC also has disease-specific gene signatures corresponding with each histological subtype: Estrogen receptor promotes EC cell proliferation ('go') and hepatocyte nuclear factor-1β (HNF-1β) induces CCC cell cycle arrest ('stop') under oxidative stress conditions. This model underscores a subtype-dependent 'go or stop' dichotomy, possibly through better ability to adapt in a changing environment. It was found that cyst fluid Hb and iron concentrations were significantly lower in EAOC when compared to benign ovarian endometrioma (OE), supporting the hypothesis that the redox imbalance plays a key role in the pathogenesis of EAOC. There are at least two phases of iron carcinogenesis and tumor progression: The initial wave of iron-induced oxidative stress and DNA mutations would be followed by the second big wave of subsequent synthesis of the antioxidants, which diminishes cellular oxidative stress capacity, increases apoptosis resistance and promotes tumor initiation and progression. Special emphasis is given to novel pathophysiological concepts of malignant transformation of endometriosis.

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Condition tags

endometriosisendometrioma

MeSH descriptors

Adenocarcinoma, Clear Cell Carcinoma, Endometrioid Cell Transformation, Neoplastic Endometriosis Ovarian Neoplasms Adenocarcinoma, Clear Cell Adenocarcinoma, Clear Cell Animals Carcinoma, Endometrioid Carcinoma, Endometrioid Cell Cycle Checkpoints Cell Cycle Checkpoints Cell Proliferation Cell Proliferation Cell Transformation, Neoplastic Cell Transformation, Neoplastic Endometriosis Endometriosis Epigenesis, Genetic Female

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 (86)

Cited by (11)

SciLite annotations

chemicals 4
heme iron iron iron

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: 2026-05-13T22:19:25.021412+00:00
scilite
last seen: 2026-05-18T04:25:29.313245+00:00
License: CC0 · commercial use OK