Risk of carcinoma in women with ovarian endometrioma

Kobayashi H, Hiroshi Kobayashi, Hirotaka Kajihara, Kajihara H, Yoshihiko Yamada, Yamada Y, Tanase Y, Yasuhito Tanase, Kanayama S, Seiji Kanayama, Furukawa N, Naoto Furukawa, Noguchi T, Taketoshi Noguchi, Haruta S, Shoji Haruta, Shozo Yoshida, Yoshida S, Katsuhiko Naruse, Toshiyuki Sado, Sado T, Hidekazu Oi, Oi H
Frontiers in bioscience (Elite edition) · 2010 · vol. E3(2) , pp. 529–540 · doi:10.2741/e267 · PMID:21196332 · W2316173048
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-08 ⓘ

This review explores the molecular genesis of endometriosis-associated epithelial ovarian carcinoma, focusing on clear cell and endometrioid subtypes and the role of oxidative stress and apoptosis in carcinogenesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 · read from full text ⓘ

This paper is a narrative review of English-language literature on the molecular genesis, pathogenesis, and pathophysiological processes underlying endometriosis-associated epithelial ovarian carcinoma (EOC), focusing on how endometriosis could transition from benign disease to carcinoma. It finds that clear cell carcinoma and endometrioid adenocarcinoma are the most frequent EOC types linked to endometriosis, and it proposes that repeated hemorrhage and retrograde menstruation introduce pro-oxidant factors such as iron, driving carcinogenesis through increased oxidative stress, DNA methylation, activation of anti-apoptotic pathways, and aberrant stress signaling. A major limitation is that it is a literature review rather than original experimental or epidemiologic analysis, and its conclusions depend on the scope of reviewed studies. This paper is centrally about endometriosis — it reviews molecular mechanisms and proposes a model for endometriosis-associated epithelial ovarian carcinoma.

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Abstract

Endometriosis affects an estimated 10% of women in the reproductive-age group. Here, we review current knowledge on molecular genesis of endometriosis-associated epithelial ovarian carcinoma (EOC). This article reviews the English language literature for biology, pathogenesis, and pathophysiological studies on endometriosis-associated EOC. Although endometriosis generally remains a benign condition, it demonstrates somatically acquired genetic alterations. Clear cell carcinoma (CCC) and endometrioid adenocarcinoma (EAC) are the most frequent types of EOC associated with endometriosis. Retrograde menstruation or ovarian hemorrhage carries highly pro-oxidant factors, such as iron, into the peritoneal cavity or ovarian endometrioma. CCC and EAC should be considered separately in studies of endometriosis-associated EOC. The repeated events of hemorrhage in endometriosis can contribute to carcinogenesis and progression via 3 major processes: 1) increasing oxidative stress promotes DNA methylation; 2) activating anti-apoptotic pathways supports tumor promotion; and 3) aberrant expression of stress signaling pathways contributes to tumor progression. This review summarizes recent advances in the understanding of epidemiology, carcinogenesis, pathogenesis, and pathophysiology of endometriosis-associated EOC; and a possible novel model is proposed.
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Abstract

Endometriosis affects an estimated 10% of women in the reproductive-age group. Here, we review current knowledge on molecular genesis of endometriosis-associated epithelial ovarian carcinoma (EOC). This article reviews the English language literature for biology, pathogenesis, and pathophysiological studies on endometriosis-associated EOC. Although endometriosis generally remains a benign condition, it demonstrates somatically acquired genetic alterations. Clear cell carcinoma (CCC) and endometrioid adenocarcinoma (EAC) are the most frequent types of EOC associated with endometriosis. Retrograde menstruation or ovarian hemorrhage carries highly pro-oxidant factors, such as iron, into the peritoneal cavity or ovarian endometrioma. CCC and EAC should be considered separately in studies of endometriosis-associated EOC. The repeated events of hemorrhage in endometriosis can contribute to carcinogenesis and progression via 3 major processes: 1) increasing oxidative stress promotes DNA methylation; 2) activating anti-apoptotic pathways supports tumor promotion; and 3) aberrant expression of stress signaling pathways contributes to tumor progression. This review summarizes recent advances in the understanding of epidemiology, carcinogenesis, pathogenesis, and pathophysiology of endometriosis-associated EOC; and a possible novel model is proposed.

Keywords

- Endometriosis - Epithelial ovarian carcinoma - Clear cell carcinoma - Stress signaling - Molecular genetics - Review

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Condition tags

endometriosisendometrioma

MeSH descriptors

Carcinoma Carcinoma Endometriosis Endometriosis Ovarian Neoplasms Ovarian Neoplasms Carcinoma Carcinoma DNA Methylation DNA Methylation Endometriosis Female Genes, ras Genes, ras Genes, Wilms Tumor Hemorrhage Hemorrhage Hemorrhage Hepatocyte Nuclear Factor 1 Hepatocyte Nuclear Factor 1

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 (71)

Cited by (19)

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