Atypical endometriosis and the progression to endometriosis-associated ovarian cancer: an updated review

P. W. Voigt, Petra C Voigt, Voigt PC, Angela Chaudhari, Chaudhari A, Susan Tsai, Tsai S, Milad MP, Magdy P. Milad, Linda Yang, Yang LC, Linda C Yang
Current opinion in obstetrics & gynecology · 2025 · vol. 37(4) , pp. 215–220 · doi:10.1097/gco.0000000000001043 · PMID:40459436 · W4410992914
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This review examines atypical endometriosis as a precursor to ovarian cancer, detailing its pathogenesis, diagnostic features like glandular crowding, and management strategies, while noting ongoing research into genomic alterations driving malignant progression.

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This review examines atypical endometriosis as a distinct histopathologic subtype that serves as a precursor lesion for endometriosis-associated ovarian cancers, specifically clear-cell and endometrioid subtypes. The authors highlight that genomic alterations and dysregulation in the mechanistic target of rapamycin pathway drive the progression from benign deep infiltrating endometriosis or ovarian endometriomas to malignancy, with glandular crowding identified as a key diagnostic feature. Although no single molecular mechanism currently predicts cancer progression, accurate pathologic diagnosis remains critical for risk characterization and guiding management strategies such as salpingo-oophorectomy. This paper is centrally about endometriosis — specifically the malignant transformation potential of atypical lesions into associated ovarian cancers.

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Abstract

PURPOSE OF REVIEW: Atypical endometriosis is a distinct subtype of endometriosis, characterized by specific histopathologic findings. It is thought to be a precursor lesion to endometriosis-associated ovarian cancers, particularly clear-cell and endometrioid subtypes, analogous to endometrial intraepithelial neoplasia as a precursor lesion to endometrial cancer. This review summarizes recent evidence regarding the pathogenesis of atypical endometriosis and progression to endometriosis-associated ovarian cancer and the diagnosis and management of atypical endometriosis. RECENT FINDINGS: (a) Pathogenesis: Deep infiltrating endometriosis and ovarian endometriomas are associated with an increased risk of ovarian cancer. Genomic alterations in endometriosis potentiate progression from benign to malignant disease. Dysregulation in the mechanistic target of the rapamycin pathway is noted throughout endometriosis and endometriosis-associated ovarian cancer. (b) Diagnosis: Glandular crowding is emphasized as an important pathologic characteristic in atypical endometriosis and appears to increase the risk of development of ovarian cancer. (c) Management: Management strategies for atypical endometriosis are guided by clinical history and imaging characteristics. SUMMARY: A strong association exists between ovarian endometriomas and deep infiltrating endometriosis and ovarian cancer. While new genomic alterations have been implicated in the progression from endometriosis to endometriosis-associated ovarian cancer, there remains no established molecular mechanism to predict cancer progression. Accurate pathologic diagnosis of atypical endometriosis is critical to characterizing ovarian cancer risk. Appropriate patient selection for salpingo-oophorectomy is the foundation of management for atypical endometriosis.
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Purpose of review Atypical endometriosis is a distinct subtype of endometriosis, characterized by specific histopathologic findings. It is thought to be a precursor lesion to endometriosis-associated ovarian cancers, particularly clear-cell and endometrioid subtypes, analogous to endometrial intraepithelial neoplasia as a precursor lesion to endometrial cancer. This review summarizes recent evidence regarding the pathogenesis of atypical endometriosis and progression to endometriosis-associated ovarian cancer and the diagnosis and management of atypical endometriosis. Recent findings (a) Pathogenesis: Deep infiltrating endometriosis and ovarian endometriomas are associated with an increased risk of ovarian cancer. Genomic alterations in endometriosis potentiate progression from benign to malignant disease. Dysregulation in the mechanistic target of the rapamycin pathway is noted throughout endometriosis and endometriosis-associated ovarian cancer. (b) Diagnosis: Glandular crowding is emphasized as an important pathologic characteristic in atypical endometriosis and appears to increase the risk of development of ovarian cancer. (c) Management: Management strategies for atypical endometriosis are guided by clinical history and imaging characteristics. Summary A strong association exists between ovarian endometriomas and deep infiltrating endometriosis and ovarian cancer. While new genomic alterations have been implicated in the progression from endometriosis to endometriosis-associated ovarian cancer, there remains no established molecular mechanism to predict cancer progression. Accurate pathologic diagnosis of atypical endometriosis is critical to characterizing ovarian cancer risk. Appropriate patient selection for salpingo-oophorectomy is the foundation of management for atypical endometriosis.

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Condition tags

endometriosisdie_deep_infiltrating

MeSH descriptors

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

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