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My research focuses on understanding the mechanisms by which tumors co-opt the immune system to facilitate emergence and progression of cancer. I am particularly interested in biology of pancreatic cancer, where non-cell-autonomous pathways elicited by oncogenic KRas and tumor suppressor p53 can modify stromal and immune responses that promote tumorigenesis. I have significant expertise in using genetically engineered mouse models of pancreatic cancer, featuring activation of oncogenic KRas in pancreatic epithelium, to investigate immunological mechanisms relevant to pathogenesis of this deadly disease. This area of research is especially pertinent in the context of KRas-driven carcinogenesis, where the driving oncogene is to this day considered an undruggable target. Our recent efforts have been directed at studying the role of B cells in cancer. We are particularly interested in understanding the mechanism behind activation and function of B cells, myeloid cells and fibroblasts in evolution of cancer and metastasis.


UNC AFFILIATIONS:

Genetics, Lineberger Cancer Center, Microbiology & Immunology

CLINICAL/RESEARCH INTERESTS:

Cancer Biology, Cell Biology, Cell Signaling, Gastrointestinal Biology, Genetics, Immunology, Translational Medicine