The principal goal of my research program is to investigate 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 use 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.