Article

Ovarian Surface Epithelium: Biology, Endocrinology, and Pathology 1

Department of Obstetrics and Gynaecology, British Columbia Women's Hospital, University of British Columbia, Vancouver, British Columbia, V6H 3V5, Canada.
Endocrine Reviews (Impact Factor: 21.06). 05/2001; 22(2):255-88. DOI: 10.1210/edrv.22.2.0422
Source: PubMed

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.

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    • "jako: • rodzinne występowanie raka jajnika, • rodzinna historia raka piersi i jajnika, • rodzinne występowanie niepolipowatego raka okrężniczo-odbytniczego (tzw. zespół Lyncha, związany z mutacjami w genach naprawy DNA: hMSH1, hMSH2, hPMS1 i hPMS2) [3]. "
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    ABSTRACT: Ovarian cancer is the most frequent cause of deaths from among gynecologic malignancies. Due to its asymptomatic development the disease is frequently diagnosed at an advanced, incurable stages. Although ovarian cancers usually respond well to the first line chemotherapy based on platinum compounds and taxanes, majority of patients develop recurrence and chemo-resistance. Despite many years of studies there is still lack of reliable diagnostic markers as well as other diagnostic methods enabling early detection and suitable for screening. Thus, current studies are aimed on finding new biomarkers with diagnostic, prognostic and predictive potential as well as on the search for the new therapeutic targets. Interestingly, an understanding of ovarian cancer etiology has changed fundamentally within recent years. The classical theory, claiming that ovarian cancers originate from ovarian surface epithelial cells, was undermined. Currently, there is a lot of evidence that majority of serous ovarian cancers have its origin in malignant tubal epithelium, while endometrioid and clear cell ovarian cancers develop most likely from endometriosis. These new findings will have an impact on diagnostic approaches as well as on the prevention options for women with genetic predisposition to ovarian cancer. The new knowledge about an origin of different histological types of ovarian cancer may open new pathways in basic research and clinical studies. In this paper we report current knowledge about ovarian cancer risk factors, we also present the arguments for extraovarian origin of the majority of ovarian cancers and stress the mechanisms of action of new drugs for targeted therapies that show most promising results in the current clinical trials.
    Full-text · Article · Dec 2015 · Postępy Higieny i Medycyny Doświadczalnej (Advances in Hygiene and Experimental Medicine)
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    • "jako: • rodzinne występowanie raka jajnika, • rodzinna historia raka piersi i jajnika, • rodzinne występowanie niepolipowatego raka okrężniczo-odbytniczego (tzw. zespół Lyncha, związany z mutacjami w genach naprawy DNA: hMSH1, hMSH2, hPMS1 i hPMS2) [3]. "

    Full-text · Article · Dec 2015 · Postępy Higieny i Medycyny Doświadczalnej (Advances in Hygiene and Experimental Medicine)
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    • "Interleukin-1 beta (IL-1í µí»½) is a proinflammatory cytokine mainly produced by monocytes and macrophages [35], but which can also be produced by endothelial cells, fibroblasts, and epidermal cells in response to bacterial or innate immunity stimulation [36]. Interestingly, normal and malignant epithelial ovarian cells also produce IL-1í µí»½ [2]. IL-1í µí»½ is translated into a 31 kDa inactive precursor form that is cleaved intracellularly by caspase-1 into an active 17 kDa secreted form [35]. "
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    ABSTRACT: Familial history remains the strongest risk factor for developing ovarian cancer (OC) and is associated with germline BRCA1 mutations, such as the 185delAG founder mutation. We sought to determine whether normal human ovarian surface epithelial (OSE) cells expressing the BRCA1 185delAG mutant, BRAT, could promote an inflammatory phenotype by investigating its impact on expression of the proinflammatory cytokine, Interleukin-1β (IL-1β). Cultured OSE cells with and without BRAT were analyzed for differential target gene expression by real-time PCR, western blot, ELISA, luciferase reporter, and siRNA assays. We found that BRAT cells expressed increased cellular and secreted levels of active IL-1β. BRAT-expressing OSE cells exhibited 3-fold enhanced IL-1β mRNA expression, transcriptionally regulated, in part, through CREB sites within the (-1800) to (-900) region of its promoter. In addition to transcriptional regulation, BRAT-mediated IL-1β expression appears dualistic through enhanced inflammasome-mediated caspase-1 cleavage and activation of IL-1β. Further investigation is warranted to elucidate the molecular mechanism(s) of BRAT-mediated IL-1β expression since increased IL-1β expression may represent an early step contributing to OC.
    Full-text · Article · Sep 2015
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