Rapid cell growth and proliferation are common features of both adaptive immunity and cancer. With the advent of targeted small molecule inhibitors for treating leukemia and lymphomas, we require a more detailed understanding of regulatory signaling involved in growth and proliferation in adaptive immune cells. The PI3K-AKT-mTOR axis stands at the center of growth and proliferation regulation, making this axis and its effectors keen targets for the development of cancer therapeutics. Moreover, PI3K-AKT-mTOR signaling plays a significant role in T and B cell activation and maturation, thus permitting specific function and regulation of this axis in immune cells. As such, many drugs which target this axis have proven to have anti-proliferative and immunomodulatory effects. For example, Rapamycin, an mTOR inhibitor initially discovered for it's antifungal effects, was found to be a potent immunosuppresive drug while paradoxically lowering the risk of cancer for certain transplant patients and improving CD8+ T cell memory.
The overarching goal of the Fruman lab is to discover PI3K-AKT-mTOR signaling components which can be targeted for therapeutic intervention in cancer and autoimmunity. My interests are in defining the mechanisms of action for the immunomodulatory and anti-proliferative effects of PI3K-AKT-mTOR targeted drugs. Insights may uncover potential mechanisms for leukemogenesis and lymphomagenesis or drug resistance in leukemia and lymphoma. Furthermore, our lab also aims to discover synergistic drug combinations for potentiating leukemia and lymphoma cell death at tolerable doses. Defining the mechanism for these combinations may also lead to safer, targeted therapies.
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