|Education||BS, University of California Irvine|
Macrophages play a large role in shaping the tumor microenvironment by driving tumor-associated inflammation. Depending on their environmental cues, they can switch between two functional phenotypes: pro-inflammatory/immunostimulatory (M1) or anti-inflammatory/immunosuppressive (M2). Our lab has shown that late stage pancreatic intraepithelial lesions (PanINs) promote the functional polarization of tumor-associated macrophages to the M2 phenotype. However, targeting the driver mutation Kras in combination with regulatory T cell depletion at the earliest stage of PanIN development can functionally reprogram these immunosuppressive cells, causing the switch to M1 phenotypes. It is clear that these two macrophage populations play important roles in defining the tumor microenvironment, but the mechanisms dictating the fates of these macrophages are not well understood. My project aims to elucidate the regulatory mechanisms of macrophage polarization both in humans and mouse models in order to find potential targets for novel immunotherapy approaches.
Yang KR, Mooney SM, Zarif JC, Coffey DS, Taichman RS, Pienta KJ. Niche inheritance: a cooperative pathway to enhance cancer cell fitness through ecosystem engineering. J Cell Biochem. 2014 Sep; 115(9):1478-85. PMID 24700698