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RPCI-Led Study: FAK Inhibitor Proves Effective Against Brain Tumors in Preclinical Studies
Date:12/29/2012

Buffalo, NY (PRWEB) December 28, 2012

Researchers from Roswell Park Cancer Institute (RPCI) have published findings from a preclinical study assessing the effectiveness of a small-molecule inhibitor, CFAK-Y15, in treating some brain cancers. The paper, published in Molecular Cancer Therapeutics, demonstrates for the first time that inhibiting the protein focal adhesion kinase (FAK) with CFAK-Y15 is an effective approach to controlling growth of glioblastoma tumors, especially in combination with the standard chemotherapy agent temozolomide (Temodar).

FAK is overexpressed, or produced in excessive amounts, in tumor cells, and has been shown to play a key role in survival of cancer cells. In this study, a team led by Vita M. Golubovskaya, PhD, an Associate Professor of Oncology in the Department of Surgical Oncology, found that animal models treated with CFAK-Y15 demonstrated significantly prolonged survival compared to the control group. CFAK-Y15 provides FAK kinase-specific inhibition by upstream targeting of autophosphorylation sites on the FAK protein. It belongs to a class of ‘two for one’ compounds that also inhibit the oncoprotein Src by inhibiting its autophosphorylation.

“We found that CFAK-Y15 significantly decreased the viability of the glioblastoma cells, and in many cases appeared to cause tumor shrinkage — especially when CFAK-Y15 was given in combination with temozolomide,” noted Dr. Golubovskaya, the paper’s first author. “These compounds target FAK signaling, which is critical for cancer cell and cancer stem cell survival, especially in invasive and metastatic cancers.”

“We’re eager to see this research move to the clinical phase because of the great need for
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