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Normal and malignant stem cells: Our lab is interested in investigating the role of chromatin regulators in benign and malignant hematopoiesis.  Several attributes of normal stem cells such as the ability to self-renew are co-opted or reactivated by cancer cells on their way to malignant transformation.  We are interested in characterizing the molecular determinants of “stemness” using hematopoietic stem cells as a model and in identifying ways and means by which these stem-cell associated pathways are usurped for oncogenesis.  



The cancer epigenome: Abnormal epigenetic changes have emerged as important mediators of oncogenesis.  Genomic investigations of human cancer have uncovered mutations in writers, erasers and readers of the histone code. The goal of our laboratory is to connect basic mechanisms of chromatin regulation to diseased states with a focus on acute myeloid leukemia (AML) and non-Hodgkin's lymphoma (NHL).  Ultimately, we are interested in the rational design of screens to develop therapeutics targeting dysregulated epigenetic mechanisms in hematological malignancies.

Gene fusions in cancer: Ever since the discovery of the Philadelphia chromosome in 1960, a number of different chromosomal translocations have been identified in human cancer, that result in the formation of potent fusion oncogenes, abnormal activation of latent proto-oncogenes, or other oncogenic events. We are very interested in investigating the impact of gene fusions on the development of human cancer. Moreover, we are also interested in understanding the propensity of certain genomic loci for recurrent involvement in oncogenic gene fusion events in human malignancies. 
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