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Mek and PI3 Inhibition in the Regulation of Pancreatic Cancer Metabolism

Last Updated:

March 25, 2015

The vast majority of pancreatic ductal adenocarcinomas (PDAC) involve activating mutations in KRAS (KRAS*) and as with other KRAS* cancers, PDAC show minimal response to existing therapies used in the clinic. While no satisfactory KRAS*-specific drugs are currently available, inhibitors of MEK and PI3K (MEKi and PI3Ki) pathways necessary for KRAS*-mediated cellular transformation in vitro are now being introduced into clinical trials.

Funded by the National Cancer Institute, the central hypothesis guiding this project is that PDAC utilize the PI3K and MEK pathways in a redundant way to drive tumor growth and that a critical role for these pathways involves the regulation of tumor metabolism. The overall goals are to determine the impact of MEKi/PI3Ki on PDAC cell signaling, metabolism and therapeutic response. These efforts will be coupled with an investigation of metabolic biomarkers for MEK/PI3K signaling and identification of mechanisms of therapeutic resistance, which would be critical in future therapeutic trials. 

Weill Cornell Medicine
Cantley Lab
Weill Cornell Medical College Meyer Cancer Center
Belfer Research Building
413 E 69th St.
Room 1362, Box 50
New York, NY 10021 Phone: (646) 962-6297