I currently serve as an Assistant Professor in the Department of Cell and Molecular Pharmacology and Experimental Therapeutics at MUSC. I received my PhD in Biochemistry and Biophysics from the University of North Carolina at Chapel Hill. I continued my studies at UNC-Chapel Hill by completing a postdoctoral fellowship in KRAS-mutant cancer signaling under the mentorship of Dr. Channing Der at the Lineberger Comprehensive Cancer Center. 

I joined the MUSC faculty in August of 2020. My postdoctoral research centered on the question of whether all KRAS mutant proteins were created equal, thereby challenging the long-standing dogma in the RAS and cancer research fields. Despite the more than 200 different RAS missense mutations found in human cancers, it was widely assumed that all RAS mutant proteins shared identical defects in function and acted similarly as cancer drivers. One KRAS mutant protein, KRAS G12R, displays an uneven prevalence among cancers that harbor the highest occurrence of KRAS mutations, suggesting context-specific properties. Our team showed that KRAS G12R was defective in regulating macropinocytosis, a metabolic process essential for PDAC tumorigenic growth. Applying biochemical, structural and cellular analyses, we determined that KRAS G12R is defective in interaction with the lipid kinase PI3Ka, a RAS effector essential for RAS-driven tumorigenesis. Our studies showed that the related PI3Kg isoform is upregulated in PDAC, independent of KRAS, enabling restoration of macropinocytosis. Finally, we established that KRAS G12R-mutant PDAC exhibits distinct therapeutic vulnerabilities. 

With the support of the DDRCC/CDLD Proteomics core and Cell Models Core, the lab will determine what makes each RAS mutant protein uniquely able to drive tumorigenesis. By utilizing a proximity ligation assay, we will determine the direct protein interactions of numerous RAS mutant proteins in both 2D and 3D cell culture, with an emphasis in determining molecular targets that can be easily transitioned to the clinic. Our longstanding goal is to develop KRAS mutation selective targeted therapies to fulfill the promise of personalized medicine while also raising the overall survival of one of the most deadly human cancers. 

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