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AMPK Directs the Balance Between Mutant Kras and PI3K Signaling and Defines Molecular Subsets in Colorectal Cancer

Scott Kopetz

5 Collaborator(s)

Funding source

University of Texas MD Anderson Cancer Center
In a collaborative project with 5 Sister Institutions and MD Anderson Investigators Dr. Scott Kopetz, and Dr. Dipen Maru, we propose a 2 year project that will: 1) allow analysis of geographically diverse colorectal cancer (CRC) and rectal cancer (RC) samples that are not readily available at MD Anderson; 2) support use these samples for a mechanistically driven proteomic study of the role of mutant KRAS and mutant PI3K in engaging different growth factor signaling pathways to elicit growth and metastasis in colorectal cancer (CRC), and 3) refine "multi-omic" classifications for CRC that incorporate these biological insights and clinical/pathologic characterizations from a diverse population. The availability of a tissue bank containing geographically diverse and early stage colon adenoma and carcinoma specimens for research purposes has always been a problem for MD Anderson because of the nature of its practice with referrals mostly Caucasian late stage CRC patients. This deficit is critical given the current effort to classify colorectal cancer into molecular subtypes.

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