George Lacaud - Overview

The AML1/Runx1 transcription factor and its cofactor CBFb, are frequent targets of gene rearrangements and mutations in human leukemias such as acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL). Consistent with its initial implication in leukemias, Runx1 has been shown to be critical for normal hematopoietic development. Runx1 deficient mice generate primitive nucleated erythrocytes, but lack all definitive erythroid and myeloid cells, indicating a complete block in definitive hematopoiesis. Using the in vitro differentiation system based on mouse embryonic stem (ES) cells, our goals are to further define the role of Runx1 in early hematopoietic development and how alterations of its function leads to leukemogenesis.