Washington University in St. Louis (WU)
DNA damage response pathways are often altered in cancer and are attractive targets for therapeutic intervention, particularly in settings where chemotherapy resistance has emerged. My laboratory studies how cells navigate a complex signaling environment following a double-strand DNA break (DSB) and ultimately engage one of several repair mechanisms. We are exploring 1) how damage signaling impacts tumorigenesis and therapy responses, and 2) how double-strand break repair proteins can be exploited as drug targets in different genetic contexts. This research is broadly centered on the idea that different genetic backgrounds impart distinct DNA repair requirements which we interrogate using advanced multiplex imaging and genomics techniques with transgenic mouse models, isogenic cell line panels, and patient-derived tumors.