My laboratory has been studying the transcriptional regulation of hematopoiesis, with the aim of understanding how the normal processes of stem cell self-renewal and differentiation are regulated and how these processes become aberrant in acute leukemia. We have been studying the AML1-ETO leukemia-promoting oncogene, defining its ability to promote stem cell self-renewal and deciphering how it regulates gene expression. We are also studying the role of epigenetic enzymes, including the protein arginine methyltransferases CARM1 and PRMT5 in normal and malignant hematopoiesis. Both CARM1 and PRMT5 can block hematopoietic stem cell (HSC) differentiation; thus they may be targeted as part of an epigenetic-based therapeutic strategy. Other work in the lab has identified a novel network of proteins, including p53, that regulate HSC quiescence and also sensitivity to chemotherapy and radiation therapy. Overall, my lab is focused on identifying novel ways to target hematologic cancers or make them more susceptible to existing therapies.