Biology of ovarian cancer.

Abstract

Although ovarian carcinomas are thought to arise from the ovarian surface mesothelial layer, the possibility that they develop from müllerian remnants within paraovarian tissues merits further consideration. Molecular genetic studies suggest that ovarian cystadenomas, low malignant potential tumors, and carcinomas are not part of a disease continuum but do represent separate disease entities. Recent advances in our understanding of the molecular genetic changes associated with ovarian epithelial tumor development can be summarized in a working genetic model for ovarian tumorigenesis, which can provide a framework for further studies. Certain molecular changes, such as telomerase expression and alterations in DNA methylation levels, are associated with both tumors of low malignant potential and carcinomas but not with cystadenomas. Mutations in the p53 gene and the development of multiple losses of heterozygosity are specific for the malignant phenotype. The nature of the specific chromosomes affected by the latter losses in a given tumor dictates its biologic aggressiveness.