Prot #STU00206173: c-Met: A Potential Target for the Treatment of Advanced Ovarian Cancer

The importance and prevalence of MET overexpression has been established in many solid tumors. Dysregulation of the MET pathway has been implicated in tumor aggressiveness, invasion, and metastasis.1 Consequently, the MET pathway is a target for novel therapeutics in many solid tumors, including non-small cell lung cancer. In ovarian cancer, the HGF/MET pathway plays a role in in the initiation and progression of disease. c-Met overexpression occurs in 30-40% of epithelial ovarian cancer cases, , and high levels of expression are associated with decreased overall survival. Targeting of the c-Met pathway in vivo decreases peritoneal dissemination and invasion in ovarian cancer cell lines.5 More recently, our team identified c-Met overexpression as a mechanism of resistance to neoadjuvant chemotherapy. The primary aim of this project is evaluate c-Met expression as a predictor of resistance to neoadjuvant chemotherapy. Our secondary aim is to investigate c-Met as an actionable target in the neoadjuvant setting in advanced ovarian cancer.