Abstract
Endometriosis is classically defined as the presence of endometrial glands and stroma outside of the endometrial lining and uterine musculature. With an estimated frequency of 5%–10% among women of reproductive age, endometriosis is a common gynecologic disorder. While in itself a benign lesion, endometriosis shares several characteristics with invasive cancer, has been shown to undergo malignant transformation, and has been associated with an increased risk of epithelial ovarian carcinoma (EOC). Numerous epidemiologic studies have shown an increased risk of EOC among women with endometriosis. This is particularly true for women with endometrioid and clear cell ovarian carcinoma. However, the carcinogenic pathways by which endometriosis associated ovarian carcinoma (EAOC) develops remain poorly understood. Current molecular studies have sought to link endometriosis with EAOC through pathways related to oxidative stress, inflammation and hyperestrogenism. In addition, numerous studies have sought to identify an intermediary lesion between endometriosis and EAOC that may allow for the identification of endometriosis at greatest risk for malignant transformation or for the prevention of malignant transformation of this common gynecologic disorder. The objective of the current article is to review the current data regarding the molecular events associated with EAOC development from endometriosis, with a primary focus on malignancies of the endometrioid and clear cell histologic sub-types.
Highlights
Network gene expression in the tumor microenvironment resulted in increased signaling related to angiogenesis, cell adhesion, cell cycle, inflammation, as well as NOTCH signaling [69]. In another microarray expression profiling study of endometriosis-associated endometrioid ovarian cancer, the expression of small inducible cytokine A2 (SICA2) and small inducible cytokine subfamily A, member 14 (CCL14) were the most up-regulated genes in endometriosis-associated endometrioid ovarian tumors when compared with benign ovaries and endometrioid cases not associated with endometriosis, suggesting that inflammatory cytokines are important in the etiology of endometriosis and associating endometrioid tumors [36]
We know that the micro-environment of endometriosis and endometriosis associated ovarian carcinoma (EAOC) share similar cytokines and mediators
Whether this similarity represents a link between endometriosis and EAOC or an employment of common signaling molecules to two separate lesions remains to be seen
Summary
Brinton et al evaluated a population-based cohort of women in Denmark between 1978 and 1998 and determined that women with endometriosis had a predisposition to ovarian cancer. This association was restricted to endometrioid (relative risk (RR) of 2.53, 95% CI; 1.19–5.38) and clear cell (RR, 95% CI; 3.37, 1.24–9.14) malignancies [19]. The objective of the current article is to review the current data regarding the genetic events and molecular changes for endometriosis-associated ovarian cancer (EAOC), with a primary focus on malignancies of the endometrioid and clear cell histologic sub-types
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