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We study the mechanisms connecting oncogenes and tumor suppressors with the biological transitions that underly step wise carcinogenesis and therapeutic response. We have a specific focus on how cancer drivers alter chromatin landscapes to establish tumor associated gene expression programs and how cancer driver mutations lead to the acquisition of genomic rearrangement. We study these mechanisms using genetically engineered mouse models of pancreatic and liver cancers that permit precise control of driver activity and that allow lineage tracing from the point that driver events are acquired.
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CLINICAL/RESEARCH INTERESTS:
Cancer Biology, Cell Biology, Cell Signaling, Developmental Biology, Drug Delivery, Epigenetics and Chromatin Biology, Gastrointestinal Biology, Genetics, Genomics, Immunology, Metabolism, Microscopy |