Tim Eubank

Background

About Tim Eubank

My research program focus is the role of myeloid cells/mononuclear phagocytes in solid tumor growth and angiogenesis as well as monocyte and macrophage HIF (hypoxia inducible factor) biology. We reported that monocytes and macrophages can be “re-educated” in solid tumors to become anti-angiogenic and were the first to report that GM-CSF stimulates tumor macrophages to overexpress the soluble form of VEGFR-1, which sequesters tumor-produced VEGF from bioactivity, and become more tumor fighting, “M1-like” depending on local tumor microenvironment. Further, we were the first to report the disparate functions of HIF-1α and HIF-2α in tumor-associated macrophages and that a hypoxia inducible factor (HIF-2α) can be anti-angiogenic. I have publications in Immunity, Blood, Cancer Research, and J of Immunology pertaining to our work in breast cancer. Further, I received the K99/R00 Pathway to Independence Award from the NCI for my work with macrophage regulation of breast cancer growth and angiogenesis. My expertise in macrophage HIF biology has led to three patent applications submitted by OSU and licensed by Akebia Therapeutics using a novel small molecule compound to stabilize HIF-2α in treatment of solid tumors. I have experience in various models of murine breast cancer (MMTV-PyMT spontaneous and orthotopic models and murine melanoma) and SCID and NSG mouse models of human cancers (HeLa, CT26, A549, MDA-MB-231, and breast cancer patient-derived xenografts). In more recent and current works, we are investigating a role for HIF-1α and HIF-2α in regulation of TIE2-expressing macrophage function, and changes in vascular perfusion to enable improved chemotherapy and radiotherapy in breast and pancreatic cancers. I have recently teamed with Brian Boone, MD, a high-volume pancreatic surgeon at WVU with expertise in neutrophils and neutrophil extracellular traps (NETs). We have projects focused on investigating the role of different macrophage subsets and their interactions with neutrophils and NETs which may dictate the immunosuppressive and hypoxic tumor microenvironment in pancreatic ductal carcinoma (PDAC). Our tools include KC and KPC mouse models of spontaneous pancreatic cancer, an orthotopic PDAC mouse model, several inducible macrophage-specific (recruited vs tissue resident) knockout mouse models, as well as PDAC patient blood and tumor samples. Other specialties: I received a Bachelors in Fine Arts from The University of Dayton and worked in the desktop publishing & printing industry for 5 years prior to making the move to graduate school and research.