Approximately 20,000 adult patients develop Acute Myeloid Leukemia (AML) each year; these patients have a ~25% chance to survive 5 years after their initial diagnosis. This is largely due to relapses, refractory disease, or serious side effects associated with current therapies (i.e. chemotherapy and/or blood stem cell transplantation). In order to develop better treatment strategies, we must first understand the underlying molecular mechanisms that initiate and maintain the disease.

Our research utilizes state-of-the-art techniques to elucidate the mechanisms that control the aberrant self-renewal and transformation of myeloid progenitor cells. A greater understanding of these processes may help us to design novel therapeutic strategies to more specifically and effectively treat AML. In addition, identifying the genes and mechanisms that control self-renewal could have important implications for regenerative medicine and stem cell biology.