Leukemia is the most common pediatric cancer, and it is among the most common causes of disease-related death in children. We are interested in understanding how mutations in blood-forming stem cells cause leukemia. We have shown that a mutation that increases stem cell numbers and causes rapid leukemia development at one stage of life may be relatively benign at another. We are working to understand how and why certain mutations have age-dependent effects on stem cells and evolving leukemia cells.
• To test whether the FLT3-Internal tandem duplication (FLT3-ITD) mutation differentially regulates the self-renewal and leukemogeneic potential of fetal, neonatal and adult hematopoietic progenitors
• To test whether FLT3-ITD activates distinct signal transduction and gene expression programs in fetal, neonatal and adult hematopoietic progenitors
Potential impact: Our overarching goal is to develop strategies to more precisely and effectively treat childhood leukemia.