More than 90% of epithelial ovarian cancers arise from single cells. Malignant transformation can be associated with a number of molecular alterations including upregulation of tyrosine kinases and phosphatases, physiologic activation of ras, mutation of p53, amplification of myc, and increased acti
Molecular pathogenesis and therapeutic targets in epithelial ovarian cancer
β Scribed by Jeremy R. Chien; Giovanni Aletti; Debra A. Bell; Gary L. Keeney; Viji Shridhar; Lynn C. Hartmann
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 275 KB
- Volume
- 102
- Category
- Article
- ISSN
- 0730-2312
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β¦ Synopsis
Abstract
Ovarian cancer, the most aggressive gynecologic cancer, is the foremost cause of death from gynecologic malignancies in the developed world. Two primary reasons explain its aggressive behavior: most patients present with advanced disease at diagnosis, and die of recurrences from disease that has become resistant to conventional chemotherapies. In this paper on epithelial ovarian cancer (EOC), we will review molecular alterations associated with the few precursor lesions identified to date, followed by the more commonly recognized processes of de novo carcinogenesis, metastasis, and the development of chemoresistance. We will propose a unifying model of ovarian epithelial tumorigenesis that takes into account various hypotheses. We will also review novel approaches to overcome the major problem of chemoresistance in ovarian cancer. Finally, we will discuss advances and new challenges in the development of mouse model systems to investigate EOC precursor lesions, progression, metastasis, and chemoresistance. J. Cell. Biochem. 102: 1117β1129, 2007. Β© 2007 WileyβLiss, Inc.
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