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The long-term goal of my research program focuses on elucidating the impact of immune dysregulation on hematologic disease and translating these findings into clinical use. Using both mouse models of disease and patient samples, we are interrogating how perturbations in signal transduction networks lead to aberrations in cell proliferation, differentiation, and/or survival in autoimmune and malignant disease. Using mice with gain or loss of function mutations in CD45, we are studying how this phosphatase, a key regulator of src family kinase activity, impacts homeostasis in the hematopoeitic system. Our translational studies in T-cell lymphoblastic leukemia and lymphoma focus on identification of novel biomarkers from patient samples that can then be used to risk stratify patients to appropriative intensity of therapy in prospective clinical trials. Hermiston, M.L., Xu, Z, Majeti, R, and Weiss, A. Reciprocal regulation of tyrosine phosphorylation by protein tyrosine kinases and protein tyrosine phosphatases. J. Clin. Invest., 109:9-14 (2002).
Hermiston, M.L., Xu, Z., and Weiss, A. CD45: A critical regulator of signal transduction thresholds in immune cells. Annual Review in Immunology, 21:107-137 (2003). Modica, R., Emergy, H., Lam, W., Hermiston, M., Grenert, J., Wirt, M., von Scheven, E. EBV associated B-cell lymphoproliferative disease in a child with NOMID. Arthritis Care and Research, 55:823-5 (2006). |
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