Rare but Still There: A Scoping Review on Endometriosis-Associated Ovarian Cancer

Karl Livori, Livori K, Calleja-Agius J, Jean Calleja-Agius, Jean Calleja‐Agius
Discovery medicine · 2024 · vol. 36(182) , pp. 467 · doi:10.24976/discov.med.202436182.44 · PMID:38531788 · W4393007367
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⚙ AI-generated summary by claude@2026-07, 2026-07-07 ⓘ

This scoping review summarizes current data on endometriosis-associated ovarian cancer, focusing on endometrioid and clear cell subtypes, their identification, prognosis, and management.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-08 · read from full text ⓘ

This scoping review summarizes existing data on endometriosis-associated ovarian cancer (EAOC), with particular attention to the endometrioid and clear cell ovarian cancer subtypes and the mechanisms proposed to link benign endometriosis to malignant transformation. It discusses investigations of interplay between endometriosis and EAOC via pathways such as oxidative stress, inflammation, hyperestrogenism, and genetic mutations in endometriotic lesions, as well as efforts to identify intermediary lesions that might enable earlier detection or prevention, while noting that EAOC’s rarity contributes to risks of late or missed diagnosis and inappropriate management with poorer prognosis. The paper’s major caveat is that the mechanisms behind EAOC development are not yet well understood. This paper is centrally about endometriosis — it focuses specifically on endometriosis-associated ovarian cancer and how endometriosis may transform into endometrioid or clear cell ovarian malignancy.

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Abstract

Endometriosis is a medical condition affecting at least up to 10% of women of reproductive age. This condition occurs when ectopic endometrial glands and stroma implant outside the uterus and there are several theories regarding the underlying origins of the disease. Endometriosis is one of the major causes of severe dysmenorrhoea, chronic pelvic pain and infertility. While endometriosis is generally a non-malignant condition, it rarely may transform into an invasive cancer, and increase the risk for epithelial ovarian cancer, notably endometrioid or clear cell ovarian cancer. Despite the increased risk, the mechanisms behind the development of endometriosis-associated ovarian cancer (EAOC) are not yet well understood. Recent investigations have delved into the intricate interplay between endometriosis and EAOC, exploring pathways involving oxidative stress, inflammation, hyperestrogenism, and the discovery of genetic mutations within endometriotic lesions that hint at a transition towards invasive carcinoma. Efforts have been made to identify intermediary lesions between endometriosis and EAOC, which may enable earlier detection of endometriosis at risk of malignant transformation or even prevention of the transformation altogether. However, given the rarity of this malignancy, there is still the risk of late or missed diagnosis, with the risk of inappropriate management being offered to the patient, and the higher risk of poor prognosis and increased morbidity and mortality. This scoping review aims to summarize existing data on EAOC, with a focus on endometrioid and clear cell histologic subtypes. It also provides insights into its identification, prognosis, and delineating management strategies, seeking to provide a holistic understanding of the complexities surrounding EAOC, facilitating further research and the development of more effective prevention and treatment approaches.
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Abstract

Endometriosis is a medical condition affecting at least up to 10% of women of reproductive age. This condition occurs when ectopic endometrial glands and stroma implant outside the uterus and there are several theories regarding the underlying origins of the disease. Endometriosis is one of the major causes of severe dysmenorrhoea, chronic pelvic pain and infertility. While endometriosis is generally a non-malignant condition, it rarely may transform into an invasive cancer, and increase the risk for epithelial ovarian cancer, notably endometrioid or clear cell ovarian cancer. Despite the increased risk, the mechanisms behind the development of endometriosis-associated ovarian cancer (EAOC) are not yet well understood. Recent investigations have delved into the intricate interplay between endometriosis and EAOC, exploring pathways involving oxidative stress, inflammation, hyperestrogenism, and the discovery of genetic mutations within endometriotic lesions that hint at a transition towards invasive carcinoma. Efforts have been made to identify intermediary lesions between endometriosis and EAOC, which may enable earlier detection of endometriosis at risk of malignant transformation or even prevention of the transformation altogether. However, given the rarity of this malignancy, there is still the risk of late or missed diagnosis, with the risk of inappropriate management being offered to the patient, and the higher risk of poor prognosis and increased morbidity and mortality. This scoping review aims to summarize existing data on EAOC, with a focus on endometrioid and clear cell histologic subtypes. It also provides insights into its identification, prognosis, and delineating management strategies, seeking to provide a holistic understanding of the complexities surrounding EAOC, facilitating further research and the development of more effective prevention and treatment approaches.

Keywords

- endometriosis - ovarian cancer - clear cell carcinoma - endometrioid carcinoma

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Condition tags

endometriosischronic_pelvic_paindysmenorrheainfertility

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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.

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