Pathology of ovarian cancer precursors

Abstract

Ninety percent of ovarian cancers in the Western world are epithelial cancers derived from the surface epithelium of the ovary and its inclusion cysts. The so-called surface epithelium is mesothelium that comes to resemble epithelium as it is reflected over the surfaces of the ovaries. At various ages, but particularly in women in the reproductive, menopausal, and postmenopausal age groups, this epithelium migrates into the ovarian stroma to form inclusion cysts. These cysts probably result from a dynamic interplay of surface epithelium and underlying ovarian stroma, but can also develop as a result of periovarian adhesions. There is abundant evidence that their formation is not related to repair of ovulation. It is generally accepted that benign and malignant ovarian epithelial tumors arise from surface epithelium and its cystic derivatives because they both, but particularly the latter, have a potential to differentiate into epithelia similar to those of normal mullerian derivation (tubal, endometrial, and endocervical epithelia) and their tumors resemble those of the fallopian tube, endometrium, and endocervix. Also, both intraepithelial carcinomas and precarcinomatous lesions can be observed in the surface epithelium and its cystic derivatives. These carcinomas may arise de nooo or as a transformation of pre-existing benign tumors and non-neoplastic lesions of similar derivation. Surface epithelial inclusion cysts have a greater propensity to undergo neoplasia than does the surface epithelium itself. This difference has been recognized for many years because most epithelial ovarian tumors are intraparenchymal, rather than being located on the ovarian surface. More recent evidence includes the immunohistochemical demonstration of various ovarian carcinoma antigens far more frequently in inclusion cyst epithelium than in surface epithelium; and the much more frequent presence of tubal metaplasia in the cyst epithelium than in the surface epithelium. Tuba1 metaplasia is encountered in non-neoplastic ovaries contralateral to ovarian carcinomas two to three times as frequently as in control ovaries, suggesting that the metaplastic epithelium is more prone to the development of carcinoma that non-metaplastic epithelium. Carcinoma precursors occur in the ovary, as in the cervix and endometrium, but have been reported only rarely because they are easily overlooked and have not been searched for by pathologists. 0 1995 Wiley Liss, Inc.Key words: Carcinoma, ovary, pathology, precursor lesions, surface epithelium Surface epithelial carcinomas account for approximately 90% of ovarian cancers in the Western world. These tumors are thought to arise either directly from the surface epithelium of the ovary and its intraparenchymal inclusion cysts or

Wnt-signalling pathway in ovarian epithelial tumours: increased expression of β-catenin and GSK3β

“…Ovarian surface epithelium is commonly believed to be the origin for ovarian adenocarcinomas, which arise in inclusion cysts lined with OSE (Scully, 1995). In our study, normal OSE lining the surface of the ovary and the inclusion cysts expressed b-catenin, GSK3b, APC and Lef-1.…”

“…They are believed to arise from inclusion cysts situated in the ovarian stroma and will typically grow in cystic formations or solid formations (Scully, 1995). The adenocarcinomas invade the nearby pelvic surroundings and later the abdomen by direct growth or via ascites fluid.…”

Inhibition of the antiproliferative effect of TGFβ by EGF in primary human ovarian cancer cells

“…Early detection of OC significantly enhances survival; however, most OCs are detected at advanced stages (Tortolero-Luna et al, 1994;Daly and Obrams, 1998). The majority of OCs arise from the ovarian surface epithelium (OSE), which are modified peritoneal mesothelial cells (Scully, 1995). A number of growth factors can regulate proliferation of the OSE, including transforming growth factor beta (TGFb), which is synthesized by normal OSE and inhibits its proliferation (Berchuk et al, 1992).…”

Cytology of human ovarian surface epithelial brushings

“…30 Most investigators agree that the HOSE is the source of this gynecologic malignancy, although others have suggested a similar role for the secondary mü llerian system at large. 2,31,32 Investigators have attempted to identify a continuum of morphologic or molecular lesions in native ovaries from atypical HOSE lesions, through cystadenomas and borderline neoplasms to frankly invasive carcinomas. 33 Atypical or dysplastic HOSE lesions have been described in ovaries prophylactically removed in otherwise healthy siblings of patients with ovarian carcinoma, as well as in ovaries removed from patients with contralateral HOSE cancer, endometrial carcinoma, and benign extraovarian disease, including polycystic ovaries.…”