ARID1A, Prostaglandin E2, and Its Receptor as Possible Predictors of Malignant Transformation of the Endometrium in Endometriosis

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Reduced ARID1A expression and lower levels of prostaglandin E2 synthase and its receptor were observed in endometrioid heterotopies, suggesting their potential as predictors of malignant transformation.

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This paper examined the expression of the tumor suppressor ARID1A, prostaglandin E2 synthase, and the prostaglandin E2 receptor in endometrium and ovarian, peritoneal, and intestinal endometrioid heterotopies from women with endometriosis of young and middle reproductive age. It reported that ARID1A expression was reduced in endometrioid heterotopies (1.2–4.0 times), with prostaglandin E2 synthase and receptor reduced more substantially (2.9–5.2 times). The authors concluded these molecules could serve as predictors of malignant transformation of endometrioid heterotopies in endometriosis, while noting the study’s limited scope to expression patterns without detailed mechanistic or longitudinal outcome validation. This paper is centrally about endometriosis — it assesses ARID1A and prostaglandin E2 pathway components as predictors of malignant transformation in endometrioid lesions associated with endometriosis.

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We studied the expression of ARID1A, prostaglandin E2 synthase, and prostaglandin E2 receptor in the endometrium and ovarian, peritoneal, and intestinal endometrioid heterotopies in women with endometriosis of young and middle reproductive age. ARID1A protein is a tumor suppressor, its expression reduced in different types of cancer. Prostaglandin E2 synthase and prostaglandin E2 receptor are involved in the signaling cascade of inflammatory reactions presumably underlying the development of endometriosis. In endometrioid heterotopies, expression of ARID1A was reduced in 1.2-4.0 times, the expression of prostaglandin E2 synthase and prostaglandin E2 receptor was reduced in 2.9-5.2 times These findings suggest that ARID1A, prostaglandin E2 synthase, and prostaglandin E2 receptor can be used as predictors of malignant transformation of endometrioid heterotopies in women with endometriosis. Similar content being viewed by others References Adamyan LV, Aznaurova YaB. Molecular aspects of endometriosis. Probl. Reprod. 2015;21(2):66-77. Russian. Bairamova NN, Protasova AE, Raskin GA, Vandeeva EN, Kuzmina NS, Yarmolinskaya MI, Orlova RV, Ovodenko DL. Endometrioid borderline ovarian tumor in the presence of endometriosis. Akush. Gin. 2018;(2):140-144. Russian. Kachalina TS, Zinov’ev AN, Zinov’eva MS, Bogatova ME. Oncological aspects of genital endometriosis. Lech. Vrach. 2017;(5):61-66. Russian. Shevchenko VE, Taipov MA, Kovalev SV, Arnotskaya NE, Pavlova OM, Kudryavtsev IA, Nikiforova ZN. Mapping of proteomic lysate of a MCF-7 cancer cell line for the identification of potential markers for breast cancer. Opukholi Zhen. Reprod. Systemy. 2012;(2):4-11. Russian. Yukhno YeA, Trofimenko IA, Trufanov GYe. Malignant transformation of endometriosis: pearls and pitfalls at magnetic resonance imaging. Opukholi Zhen. Reprod. Systemy. 2013;(3-4):72-80. Russian. Bedaiwy MA, Allaire C, Yong P, Alfaraj S. Medical management of endometriosis in patients with chronic pelvic pain. Semin. Reprod. Med. 2017;35(1):38-53. Guan B, Mao TL, Panuganti PK, Kuhn E, Kurman RJ, Maeda D, Chen E, Jeng YM, Wang TL, Shih IeM. Mutation and loss of expression of ARID1A in uterine low-grade endometrioid carcinoma. Am. J. Surg. Pathol. 2011;35(5):625-632. Guan B, Wang TL, Shih IeM. ARID1A, a factor that promotes formation of SWI/SNF-mediated chromatin remodeling, is a tumor suppressor in gynecologic cancers. Cancer Res. 2011;71(21):6718-6727. Paltsev MA, Polyakova VO, Kvetnoy IM, Anderson G, Kvetnaia TV, Linkova NS, Paltseva EM, Rubino R, De Cosmo S, De Cata A, Mazzoccoli G. Morphofunctional and signaling molecules overlap of the pineal gland and thymus: role and significance in aging. Oncotarget. 2016;7(11):11,972-11,983. Rafique S, Decherney AH. Medical management of endometriosis. Clin. Obstet. Gynecol. 2017;60(3):485-496. Takeda T, Banno K, Okawa R, Yanokura M, Iijima M, Irie-Kunitomi H, Nakamura K, Iida M, Adachi M, Umene K, Nogami Y, Masuda K, Kobayashi Y, Tominaga E, Aoki D. ARID1A gene mutation in ovarian and endometrial cancers (Review). Oncol. Rep. 2016;35(2):607-613. Wiegand KC, Shah SP, Al-Agha OM, Zhao Y, Tse K, Zeng T, Senz J, McConechy MK, Anglesio MS, Kalloger SE, Yang W, Heravi-Moussavi A, Giuliany R, Chow C, Fee J, Zayed A, Prentice L, Melnyk N, Turashvili G, Delaney AD, Madore J, Yip S, McPherson AW, Ha G, Bell L, Fereday S, Tam A, Galletta L, Tonin PN, Provencher D, Miller D, Jones SJ, Moore RA, Morin GB, Oloumi A, Boyd N, Aparicio SA, Shih IeM, Mes-Masson AM, Bowtell DD, Hirst M, Gilks B, Marra MA, Huntsman DG. ARID1A mutations in endometriosis-associated ovarian carcinomas. N. Engl. J. Med. 2010;363(16):1532-1543. Zhu J, Mayr D, Kuhn C, Mahner S, Jeschke U, von Schönfeldt V. Prostaglandin E2 receptor EP1 in healthy and diseased human endometrium. Histochem. Cell Biol. 2018;149(2):153-160. Author information Authors and Affiliations Corresponding author Additional information Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 167, No. 4, pp. 493-496, April, 2019 Rights and permissions About this article Cite this article Dyatlova, A.S., Lin’kova, N.S., Polyakova, V.O. et al. ARID1A, Prostaglandin E2, and Its Receptor as Possible Predictors of Malignant Transformation of the Endometrium in Endometriosis. Bull Exp Biol Med 167, 504–507 (2019). https://doi.org/10.1007/s10517-019-04560-7 Received: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s10517-019-04560-7

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endometriosis

MeSH descriptors

Dinoprostone DNA-Binding Proteins Endometriosis Transcription Factors Adult Cell Transformation, Neoplastic Cell Transformation, Neoplastic Cell Transformation, Neoplastic Dinoprostone Dinoprostone DNA-Binding Proteins DNA-Binding Proteins Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans Transcription Factors

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