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Abstract

Abstract 

  1. Ovarian carcinomas are the fifth leading cause of death from cancer among women. These tumors are morphologically similar to those arising from Müllerian-derived gynecologic organs despite the ovary itself not being embryologically derived from Müllerian ducts.

  2. That ovarian carcinomas rarely spread outside the pelvic and abdominal cavities should facilitate usage of molecular genetic tests to document the presence or absence of residual tumor cells in treated patients.

  3. Ovarian carcinomas are thought to arise from the mesothelial layer lining the ovarian surface. This theory does not account for the Müllerian-like appearance of these tumors and remains unproven.

  4. The development of a suitable animal model for ovarian carcinomas is complicated by the low frequencies of these tumors in lower mammals. That such tumors are associated with frequent ovulation in birds supports theories linking incessant ovulation to risk of ovarian cancer in humans.

  5. In vitro cultures of cells regarded as possible candidates for the origin of ovarian carcinomas, as well as of benign ovarian tumors, are available. Such cultures provide experimental systems to clarify the association between these different cell types and ovarian tumorigenesis.

  6. Ovarian epithelial tumors are a good model to study tumor development because they are subdivided into benign, low malignant potential, and different grades of malignant subgroups which can each be regarded as representing varying degress of neoplastic transformation.

  7. Although most ovarian carcinomas occur sporadically, a significant proportion arise in individuals with familial predisposition to this disease. The best-characterized genetic determinants of such predisposition are inherited mutations in either the BRCA1 gene (familial breast/ovarian cancer syndrome) or in genes coding for mismatch repair enzymes (Lynch II syndrome).

  8. Molecular genetic changes distinguishing ovarian cystadenomas, LMP tumors, and different grades of carcinomas from each other have been described. A gene that possibly escapes X chromosome inactivation may control the development of tumors of low malignant potential. Abnormalities in the same gene may be associated with increased biological aggressiveness in carcinomas.

  9. Molecular genetic studies suggest that benign and malignant ovarian epithelial tumors are usually not part of a disease continuum. Benign tumors that progress to malignancy are probably those that are predisposed to such progression from their onset because of the presence of molecular genetic abnormalities associated with malignancy.

  10. A genetic model for ovarian epithelial tumor development can be formulated based on known molecular genetic differences between benign, low malignant potential, and malignant tumors.

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