Our Research (under construction)

We study the mechanism of leukemogenesis with the long term goal of developing more effective therapeutic agents that target the leukemic stem cells (LSC). Normal hematopoiesis typically displays a balanced program of self-renewal, proliferation and differentiation of hematopoietic stem cells (HSC) and progenitors. Mutations that activate oncogenes or inactivate tumor suppressor genes disrupt this balance and cooperate to transform HSC or progenitors into leukemic initiating cells. We use mouse models that faithfully recapitulate human leukemia to study how oncogenes and tumor suppressor genes dysregulate HSC and progenitors to promote leukemogenesis. 

Some areas of research interests:
1. metabolic regulation of HSC function under normal and diseased conditions
2. ER stress signaling and protein quality control in HSCs under normal and disease conditions
3. Ras signaling in leukemogenesis