My laboratory has two main research areas: Mechanisms of T cell leukemogenesis and the role of RIP kinases in TNF- and TLR- signaling and cell death. We use the mouse as a model system to interrogate the pathways that control inflammation and to understand the genetic basis of T cell acute lymphoblastic leukemia (T-ALL).
T cell acute lymphoblastic leukemia (T-ALL) is largely caused by the activation of the TAL1, LMO1/2, and the NOTCH1 oncogenic pathways. The overall goal of of this research program is to understand how the TAL1 and NOTCH1 pathways give rise to T-ALL and to use this mechanistic knowledge to design new therapeutic approaches.
The serine/threonine kinase RIPK1 is recruited to the TNF receptor 1 to mediate proinflammatory signaling and to regulate TNF-induced cell death. The goal of this research program is to use the novel mouse models we have developed to reveal the tissue specific roles for RIPK1 in cell survival and host defense.