{"paper_id":"75fcad85-7b3f-4871-a082-cf290d1e19a2","body_text":"Copyright© 2025 The Author. Published by Galenos Publishing House on behalf of European Society for Gynaecological Endoscopy. \nThis is an open-access article under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) License.\n3\nEDITORIAL\nFacts Views Vis Obgyn 2025;17(1):3-4\nIs it time to re-evaluate how we speak to women with \nendometriosis about their risk of ovarian cancer\n Thomas Edward Ind\nHead of Department of Gynaecological Oncology, Royal Marsden Hospital, London, United Kingdom\nKeywords: Endometriosis, endometriomas, ovarian cancer\nThe lifetime risk of all ovarian cancers in women is \nabout 1.3% (1 in 77), with that reported in women \nwith endometriosis to be 1.8% (1 in 56). 1 A more \nrecent meta-analysis confirmed the association, \nwith the strongest relationship occurring with type 1 \nhistological subtypes.2 There is a 160% increased risk \nof cardiovascular disease if a woman is menopausal, \naccompanied by the risks of surgery, most authors feel \nthat the increased risk of ovarian cancer secondary to \nendometriosis does not warrant surgical intervention. \nRecent ESHRE guidelines state that “... clinicians \nreassure women with endometriosis with regards to \ntheir cancer risk...”.3\nHowever, the same guideline states that “... \nthere is epidemiological data, mostly on ovarian \nendometriosis, showing that complete excision of \nvisible endometriosis may reduce the risk of ovarian \ncancer...”.3\nThe association between endometriosis and ovarian \ncancer is greater than the proportion of cases that fulfil \nthe Sampson criteria 4 for Endometriosis Associated \nOvarian Cancer (EAOC) and is thought to be related \nto combinations of inflammation, oxidative stress, \noestrogens, and genomic alteration via the KRAS, \nP13K pathways with alteration in ARID1A and PTEN. For \nthis reason, we more commonly associate EAOC with \nclear cell, endometrioid, and low-grade serous types \nof cancers (type 1) with odds ratios previously being \nreported as high as 3.73, 2.32, and 2.02, respectively.5\nA more recent study has looked at the ‘typology’ \nof endometriosis and the ovarian cancer risk by \nassessing 78,476 women with endometriosis on the \nUtah Population Database matched against those \nwomen without endometriosis on a 1 to 5 ratio. 6 In \nthis later study, the median follow-up in women with \nendometriosis was 8 years and 14 years for women \nwithout endometriosis. The adjusted hazard ratio for \nany endometriosis and the development of epithelial \novarian cancer was 4.20 [confidence interval (CI): 3.59-\n4.91)].\nHowever, women with deep infiltrative endometriosis \nand endometriomas had the highest hazard ratios for \nepithelial ovarian cancer of 9.66 (CI: 7.77-12.00). This \nincreased risk involved all epithelial ovarian cancers, \nincluding high-grade serous carcinomas, which have \npreviously not been associated with endometriosis. \nThe adjusted hazard ratio for type 1 ovarian cancers \nwas 18.96 (CI: 13.78-26.08).\nCorresponding Author: Thomas Edward Ind, MD, Head of Department of Gynaecological Oncology, Royal Marsden Hospital, \nLondon, United Kingdom\nE-mail: ThomasInd@mac.com ORCID ID: orcid.org/0000-0001-5260-199X\nReceived: 31.07.2024 Accepted: 15.12.2024 Publication Date: 28.03.2025\nCite this article as: Ind TE. Is it time to re-evaluate how we speak to women with endometriosis about their risk of ovarian \ncancer. Facts Views Vis Obgyn. 2025;17(1):3-4\nDOI: 10.52054/FVVO.2024.13577\n\nFacts Views Vis Obgyn 2025;17(1):3-4\n4\nAs with other registry-based studies, the Utah Study’s \nstrength lies in the large number of patients. 6 However, \nthe diagnosis of endometriosis itself is not a rigorous \none, with some patients diagnosed on symptoms \nalone, others by laparoscopic interpretation and others \nby histology. Histologically proven endometriosis can \nbe in a number of different sites and can be superficial \nor deep, or it can be in the form of endometriomas. \nRegistry-based clinical studies are not without their own \ninstrinsic failings.\nThey often lack in data quality and are variable in detail. \nFurthermore, there are often failings in active follow-\nup.7 In this subject, known confounding factors such \nas contraceptive pill usage and tubal ligation are not \naccounted for.\nThe significance of any new data lies in how practice \ncould change as a result. With type 1 ovarian cancers \naccounting for about 20% of all cases and therefore \noccurring in about 1 in 400 women, even with a hazard \nratio of nearly 20, any intervention could result in at best \n20 people receiving treatment to prevent one case. Either \nway, this could be presented in plain language to a patient \nwishing to make an informed decision and balanced \nalong with symptoms, fertility wishes and risks of surgery. \nThere is some evidence that excision of endometriosis \n(especially endometriomas) may be protective against \nthe risk of EAOC. 8,9 However, the extent of protection \nis controversial and does not take into account other \nenvironmental factors and hormone usage that may also \ninfluence malignant transformation.\nThis study will no doubt prompt analyses of other large \npatient cohorts. If these figures are confirmed, then we \nwill have to rethink how we counsel women with a history \nof deep infiltrative endometriosis and endometriomas. \nThis is especially in those women who are nearing the \nend of their menstrual life and who have completed their \nfamily. Furthermore, an understanding of the molecular \ndifferences between women with endometriosis that \neventually do lead to EAOC and those that do not might \nhelp us understand which patients to offer prophylactic \nsurgery to.\nAcknowledgements: None.\nFootnotes\nFinancial Disclosure: The author declared that this study received no \nfinancial support.\nReferences\n1. Kvaskoff M, Horne AW, Missmer SA. Informing women with \nendometriosis about ovarian cancer risk. Lancet. 2017;390:2433-4.\n2. Kvaskoff M, Mahamat-Saleh Y, Farland LV , Shigesi N, Terry KL, Harris \nHR, et al. Endometriosis and cancer: a systematic review and meta-\nanalysis. Hum Reprod Update. 2021;27:393-420.\n3. Becker CM, Bokor A, Heikinheimo O, Horne A, Jansen F , Kiesel \nL, et al. ESHRE guideline: endometriosis. Hum Reprod Open. \n2022;2022:hoac009. \n4. Sampson JA. Metastatic or embolic endometriosis, due to the \nmenstrual dissemination of endometrial tissue into the venous \ncirculation. Am J Pathol. 1927;3:93-110.43.\n5. Pearce CL, Templeman C, Rossing MA, Lee A, Near AM, Webb PM, \net al. Association between endometriosis and risk of histological \nsubtypes of ovarian cancer: a pooled analysis of case-control \nstudies. Lancet Oncol. 2012;13:385-94.\n6. Barnard ME, Farland LV , Yan B, Wang J, Trabert B, Doherty JA, \net al. Endometriosis typology and ovarian cancer risk. JAMA. \n2024;332:482-9.\n7. Rubinger L, Ekhtiari S, Gazendam A, Bhandari M. Registries: big \ndata, bigger problems? Injury. 2023;54(Suppl 3):S39-S42.\n8. Haraguchi H, Koga K, Takamura M, Makabe T, Sue F , Miyashita M, et \nal. Development of ovarian cancer after excision of endometrioma. \nFertil Steril. 2016;106:1432-7.e2.\n9. Melin AS, Lundholm C, Malki N, Swahn ML, Sparèn P , Bergqvist A. \nHormonal and surgical treatments for endometriosis and risk of \nepithelial ovarian cancer. Acta Obstet Gynecol Scand. 2013;92:546-\n54.","source_license":"CC0","license_restricted":false}