| Barbara L. Kee, Ph. D. Assistant Professor Department of Pathology Committees on Immunology, Cancer Biology and Developmental Biology University of Chicago 5841 S. Maryland Ave., MC1089 Chicago IL 60637 Phone: 773-702-4349 Fax: 773-834-5251 email: bkee@bsd.uchicago.edu Ph.D., University of Toronto 1995 B.Sc., University of Toronto 1989 Post-doc: UC San Diego 1996-2001 |
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| Research Interests: My lab is interested in determining the basic mechanisms that regulate lymphocyte development from hematopoietic stem cells. We have focused on identifying the network of transcriptional regulatory proteins that establish distinct cell lineages. We are also interested in determining how these networks interact with other regulatory pathways in the cell including growth factor and cytokine signaling and how these integrated networks control cell fate. Much of our work has centered on the transcription factors encoded by the E2A gene, which are required for proper development of B- and T-lymphocytes. We have defined the essential targets of E2A that promote B lineage specification (Early B cell Factor, EBF) and expansion (N-myc) in response to cytokines. Current projects are directed at identifying the transcriptional networks involved in natural killer cell and T-lymphocyte lineage specification, as well as lymphoid specification from hematopoietic stem cells. A second area of interest in the lab is to understand the mechanisms leading to lymphoid malignancies. Multiple conserved regulatory networks that promote hematopoietic stem cell or lymphocyte survival and proliferation are aberrantly regulated in T cell lymphoma. We have found that lymphomas arising in E2A-deficient mice invariably have mutations in the Notch1 transmembrane receptor that lead to prolonged and heightened activation, and these tumors require Notch1 signaling for their survival. We are currently characterizing the Notch1 target genes that promote transformation of lymphocytes and we are determining how Notch1 and other oncogenic proteins become de-regulated in E2A-deficient thymocytes. |