{"paper_id":"5091ca7b-6323-4c22-96a2-b0a7dbf16de6","body_text":"Zusammenfassung\nEndometriose ist eine häufige benigne Erkrankung mit einer Prävalenz von ca. 10% bei Frauen in der reproduktiven Phase ihres Lebens. Das Risiko, ein endometrioseassoziiertes Ovarialkarzinom (EAOC) zu entwickeln, ist für Frauen mit Endometriose im Vergleich zu Frauen ohne Endometriose etwa verdoppelt. Besteht zusätzlich zur Endometriose noch eine langjährige Infertilität, ist das Risiko für ein EAOC sogar vervierfacht. Retrospektive Studien haben eine histopathologische Korrelation zwischen Endometriose und EAOC aufzeigen können. Neuere Untersuchungen beschäftigen sich mit molekularbiologischen Methoden, um neue Aspekte der Pathophysiologie zu beschreiben. Einen möglichen Einfluss auf die Entstehung eines Ovarialkarzinoms aus der Endometriose haben inflammatorische Faktoren innerhalb des Peritonealmilieus, Angiogenese, Hyperöstrogenismus, Aromatasestoffwechsel, Cyclooxygenase-2 und der Verlust von genetischem Material, wie z. B. die Inaktivierung von Tumorsuppressorgenen. Es besteht die Hoffnung, durch neue molekularbiologische Untersuchungen die Inzidenz der EAOC zu reduzieren.\nAbstract\nEndometriosis is a common benign disease with a prevalence of about 10% in the female population during the reproductive phase. The risk of developing endometriosis-associated ovarian cancer (EAOC) is doubled for women with endometriosis in comparison to the risk of women without endometriosis developing ovarian cancer. If patients with endometriosis suffer additionally from long lasting infertility, the risk for EAOC is even increased four times. Retrospective studies have shown a histopathological correlation between endometriosis and EAOC. Recent investigations focus on the molecular biological methods used to describe new aspects of the pathophysiology of this disease. The formation of EAOC seems to be influenced by inflammation within the peritoneal cavity, angiogenesis, hyperestrogenism, the aromatase pathway, cyclooxygenae-2 and loss of genetic material such as the inactivation of tumor suppressor genes. Such molecular biological investigations may reduce the incidence of EAOC.\nSimilar content being viewed by others\nLiteratur\nBenoit L, Arnould L, Cheynel N et al. (2006) Malignant extraovarian endometriosis: a review. Eur J Surg Oncol 32(1): 6–11\nBrinton LA, Gridley G, Persson I et al. (1997) Cancer risk after a hospital discharge diagnosis of endometriosis. Am J Obstet Gynecol 176(3): 572–579\nBrinton LA, Westhoff CL, Scoccia B et al. (2005) Causes of infertility as predictors of subsequent cancer risk. Epidemiology 16(4): 500–507\nCastiblanco GA, Pires NY, Wistuba OI et al. 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Gynäkologische Endokrinologie 4, 133–136 (2006). https://doi.org/10.1007/s10304-006-0152-y\nIssue date:\nDOI: https://doi.org/10.1007/s10304-006-0152-y\nSchlüsselwörter\n- Endometriose\n- Endometrioseassoziierte Ovarialkarzinome\n- Maligne Transformation\n- Inflammation\n- Tumorsuppressorgene","source_license":"CC0","license_restricted":false}