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. 2020 Dec;8(24):1712. doi: 10.21037/atm-20-3022a

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2020 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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Hypothetic model of pathogenesis of endometriosis-associated ovarian carcinoma. Reactive oxygen species (ROS) due to free heme and catalytic iron contained in the trapped blood in endometriomas may lead to increased oxidative stress and DNA damage in the epithelial layer of endometriomas. This may result in mutations and epigenetic changes, including mutations in the tumor suppressor gene ARID1A and possible second-hit mutations as well as activation of the PI3K-AKT-mTOR pathway to escape apoptosis caused by increased oxidative stress. The accumulation of oncogenic mutations in atypical endometriosis may ultimately lead to the development of endometriosis-associated ovarian clear cell (OCC) and endometrioid (EnOC) carcinomas (adapted from Vercellini et al., Hum Reprod, 2011 and Samartzis et al., GYNÄKOLOGIE, 2018).