Abstract
Ovarian cancer is the most lethal of all of the gynecological cancers and can arise from any cell type of the ovary, including germ cells, granulosa or stromal cells. However, the majority of ovarian cancers arise from the surface epithelium, a single layer of cells that covers the surface of the ovary. The lack of a reliable and specific method for the early detection of epithelial ovarian cancer results in diagnosis occurring most commonly at late clinical stages, when treatment is less effective. In part, the deficiency in diagnostic tools is due to the lack of markers for the detection of preneoplastic or early neoplastic changes in the epithelial cells, which reflects our rather poor understanding of this process. Animal models which accurately represent the cellular and molecular changes associated with the initiation and progression of human ovarian cancer have significant potential to facilitate the development of better methods for the early detection and treatment of ovarian cancer. This review describes some of the experimental animal models of ovarian tumorigenesis that have been reported, including those involving specific reproductive factors and environmental toxins. Consideration has also been given to the recent progress in modeling ovarian cancer using genetically engineered mice.
Highlights
Despite improved knowledge of the etiology of ovarian cancer, aggressive cytoreductive surgery, and modern combination chemotherapy, there has been little change in the mortality statistics over the last 30 years, and approximately 60% of the women who develop ovarian cancer will die from their disease
Ovarian cancer cell lines derived from ascites or primary ovarian tumors have been used extensively and can be very effective for studying the processes controlling growth regulation and chemosensitivity
The ideal model to investigate the pathogenic events associated with early ovarian tumorigenesis would be a mouse model in which the tumor arises directly from the ovarian surface epithelium (OSE) cells
Summary
Despite improved knowledge of the etiology of ovarian cancer, aggressive cytoreductive surgery, and modern combination chemotherapy, there has been little change in the mortality statistics over the last 30 years, and approximately 60% of the women who develop ovarian cancer will die from their disease. The incidence of ovarian cancer climbs dramatically in women around the age at which they reach menopause The reason for this is not clear, but two of the major changes associated with menopause form the foundation for hypotheses regarding the origin of ovarian tumors: 1) the depletion of oocytes or germ cells, which is the underlying cause of menopause, and 2) a significant increase in the pituitary's production of the gonadotropic hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), that arises as a consequence of the reduced follicular estrogen levels. The ideal model to investigate the pathogenic events associated with early ovarian tumorigenesis would be a mouse model in which the tumor arises directly from the OSE cells This model would differ from current xenograft models in that transgenic mice with defined genetic lesions could be studied at various stages as they inevitably develop ovarian cancer in situ. The demonstration that the MISIIR promoter can be used successfully to drive gynecological tissue-specific transgene expression in mice and that this often results in the formation of ovarian carcinoma offers very promising opportunities for testing the efficacy of chemotherapeutic and chemopreventive agents in a heritable model of epithelial ovarian cancer
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