Characterization of signaling routes downstream of oncogenic KRAS

© C. Scholl

The most commonly mutated oncogenes in human cancer are the members of the RAS gene family, with KRAS mutations found in ~30% of malignant tumors. One main goal of our research is to identify and characterize previously unrecognized effectors and regulatory networks that are engaged by mutant KRAS to transmit its oncogenic properties. This approach has the potential to uncover genotype-specific vulnerabilities that could serve as novel therapeutic targets.


For example, we are using technologies such as large-scale proteomics and functional genomic screens (RNA interference or CRISPR/Cas9 technology) to uncover signaling networks and potentially druggable “Achilles’ heels” in KRAS mutant cancer cells. In addition, by exploiting genetically engineered mouse models, we are investigating the physiological and oncogenic function of Stk33, an uncharacterized serine/threonine kinase that we found to be essential for the survival of mutant KRAS-dependent cancer cells (Scholl et al. Cell 2009; Azoitei et al. J Exp Med 2012).


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