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In our research program, we explore parallel opportunities for novel cancer therapy by
Targeting signal transduction: S6K1.
S6K1 is a protein kinase that is activated in response to some of the most frequently occuring mutations in across the cancer spectrum. Inactivating mutations in the critcal tumor suppressor protein PTEN, or activating mutations in proto-oncogenes such as PI3K, ultimately activate robust S6K1 signaling. Despite the frequent activation of S6K1 in human cancer, the opportunities for cancer therapy by targeting S6K1 are underexplored. We conduct experiments in validation and pre-clinical development of S6K1 as a target using genetic and pharmacologic approaches in glioblastoma, leukemia, and other cancers.
Targeting metabolism: Metabolic adaptive responses.
Some cancer cells can rewire their metabolic function to adapt to chemotherapy. These Metabolic Adaptive Responses allow the cancer cell to survive during chemotherapy stress by accessing alternative carbond sources. In our studies of tumor cell metabolism, we focus on the role of Fatty Acid Oxidation in mediating resistance to signaling pathways targeted therapeutics. Experiments are focused on identifying and targeting the mechanisms that permit Metabolic Adaptive Responses in cancer.
Recruiting anti-tumor immune responses.
Tumor immunology is revolutionizing cancer therapy. In new work for our group, we are beginning to explore how specific oncogenic mutations influence tumor-intrinsic production of immune-modulatory ligands. We aim to better understand how to incorporate anti-tumor immune responeses into a regimen that includes the three traditional arms of cancer therapy: surgery, radiation, and chemotherapy.
Vontz Center for Molecular Studies 3125 Eden AvenuePO Box 670521Cincinnati, OH 45267-0521
Mail Location: 0521Phone: 513-558-5323Fax: 513-558-1190Email: cbrecruitment@uc.edu