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Our laboratory's research is focused on defining the molecular basis of human carcinogenesis. Our studies can be divided into three broad areas. First, we are interested in delineating the mechanism by which the Ras oncoprotein promotes malignant transformation. Second, we are pursuing studies to determine the contribution of Ras-related proteins, specifically, the Rho GTPases, to oncogenesis. Third, our studies also involve approaches to identify novel oncogenes involved in the development of human leukemias and carcinomas.

Mutated forms of the Ras oncoprotein are found in 30% of all human cancers. In normal cells, Ras functions as a molecular switch that relays the stimuli initiated by many different extracellular signals to cytoplasmic signaling pathways. These signaling pathways in turn regulate normal cell proliferation, differentiation, and cell survival. The mutated Ras proteins found in cancer cells are chronically-activated proteins. Hence, they stimulate signaling in the absence of extracellular stimuli in a persistent and uncontrolled fashion.


NIH 3T3 mouse fibroblasts transfected with GFP-tagged K-Ras 12V

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