Most high grade serous carcinomas are characterized by TP53 mutations and lack of mutations of KRAS, BRAF, or ERBB2, Mutant p53 is almost invariably existing and plays a essential purpose while in the mole cular pathogenesis of large grade serous carcinoma, In recent years, RTK targeted cancer therapies such as, anti ERBB2 in breast cancer, anti KIT and PDGFA in gastrointestinal stromal tumors, anti BCR ABL in chronic myelogenous leukemia and anti EGFR in non small cell lung cancer have viewed widespread clinical use. Nevertheless, regardless of the abovementioned evidence for tyrosine kinase activation in ovarian cancer pathogenesis, targeted anti kinase therapies just had only minimal or partial clinical response in sufferers with ovarian cancer, During the present research we show the simultaneous activation of numerous selleck chemical RTKs which include EGFR, ERBB2, MET, and or AXL in selleck Dabrafenib individual ovarian cancer cell lines and principal tumors. We also showed that HSP90 inhibition is a compelling method to inactivate multi ple RTKs. The inhibition of multiple RTKs had superior effect in maximizing apoptosis and anti proliferation when compared to the inactivation of any single RTK inhibi tion in these models.