Ovarian Surface Epithelium: Biology, Endocrinology, and Pathology

Abstract

The epithelial ovarian carcinomas, which make up more than 85% of human ovarian cancer, arise in the ovarian surface epithelium (OSE). The etiology and early events in the progression of these carcinomas are among the least understood of all major human malignancies because there are no appropriate animal models, and because methods to culture OSE have become available only recently. The objective of this article is to review the cellular and molecular mechanisms that underlie the control of normal and neoplastic OSE cell growth, differentiation, and expression of indicators of neoplastic progression. We begin with a brief discussion of the development of OSE, from embryonic to the adult. The pathological and genetic changes of OSE during neoplastic progression are next summarized. The histological characteristics of OSE cells in culture are also described. Finally, the potential involvement of hormones, growth factors, and cytokines is discussed in terms of their contribution to our understanding of the physiology of normal OSE and ovarian cancer development.

The E3 ubiquitin ligase EDD is an adverse prognostic factor for serous epithelial ovarian cancer and modulates cisplatin resistance in vitro

“…EDD was expressed in almost all of the carcinomas examined (n ¼ 149/151, 98.7%), with 57.6% (n ¼ 87/151) classified as having high nuclear expression of EDD (overall score X6) ( Table 1). EDD expression in undiseased (normal) ovarian surface epithelium or inclusion cysts, small foci of hyperplastic epithelium found within the cortex of normal ovaries and proposed as the site of origin of epithelial ovarian tumours (Auersperg et al, 2001), was rare (Figure 1). There was no association between EDD staining and any of the clinicopathological or gene expression variables tested, with the exception of preoperative serum CA125 levels ( Table 2).…”

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

“…The downregulation of cadherins or dysfunction of the cadherincatenin complex has been noted in different types of tumours. In the human ovary, neuronal (N) cadherin, but not epithelial (E) cadherin, is expressed in the normal ovarian surface epithelium (OSE) (Sundfeldt et al, 1997;Auersperg et al, 2001). However, Ecadherin is upregulated in inclusion cysts of the normal ovary and in ovarian tumours with invasive capacity (Sundfeldt et al, 1997;Auersperg et al, 2001).…”

“…In the human ovary, neuronal (N) cadherin, but not epithelial (E) cadherin, is expressed in the normal ovarian surface epithelium (OSE) (Sundfeldt et al, 1997;Auersperg et al, 2001). However, Ecadherin is upregulated in inclusion cysts of the normal ovary and in ovarian tumours with invasive capacity (Sundfeldt et al, 1997;Auersperg et al, 2001). At the protein level, both a-and b-catenin are expressed in normal OSE and invasive ovarian tumours (Auersperg et al, 2001 types of ovarian tumours (Gamallo et al, 1999;Wright et al, 1999).…”

Five different phenotypes of endothelial cell cultures from the bovine corpus luteum: Present outcome and role of potential dendritic cells in luteolysis

“…Understanding the function of the CK + surface epithelium cells meets a continuous interest because of the ongoing debate on the origin of epithelial ovarian cell cancer (Auersperg et al, 2001;Kumar et al, 2009). On the contrary, the study of CK + follicle cells is widely neglected.…”