ON THE RISKS OF MALIGNISATION OF OVARIAN ENDOMETRIOMAS

Р. И. Габидуллина, F. F. MINNULLINA, DINARA I. AKHMETOVA, ALIYA SH. ZARIPOVA, KAMILYA I. ZIDIHANOVA, DARYA A. ROOT
In: The Bulletin of Contemporary Clinical Medicine · 2023 · vol. 16(4) , pp. 78–82 · doi:10.20969/vskm.2023.16(4).78-82 · W4387933986
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This review analyzes epidemiological and genetic studies from 2012-2023, confirming an increased risk of ovarian and endometrial cancers in women with endometriosis, particularly clear-cell and endometrioid ovarian cancers.

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Abstract

Introduction. Endometriosis is a widespread gynecological disease. In the last few years, new data have been accumulating confirming that endometriosis leads to an increased risk of malignant neoplasms of the ovaries, endometrium, breast and thyroid gland. The most commonly found form of endometriosis is endometrioma. Objective: to analyze epidemiological and genetic studies of the risks of neoplastic transformation of ovarian endometriomas based on search results in electronic resources MEDLINE, EMBASE, Elibrary from 2012 to 2023. Results. Epidemiological and genetic studies have proven the risk of malignancy of endometriosis with the development of ovarian cancer related to endometriosis. Studies confirmed, that two histotypes of epithelial ovarian cancer, such as clear-cell and endometrioid cancer, most closely related to endometriosis. Genome-wide association studies (GWAS) have confirmed the risk of endometrial cancer in women with endometriosis, which was shown earlier than epidemiological studies. Finding the genes and pathways underlying these complex diseases is an essential step toward developing better diagnostic and therapeutic tools. Conclusion. The review presents epidemiological and genetic evidence of the risks of ovarian cancer and endometrial cancer in women with endometriosis.

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endometriosisendometrioma

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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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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