Disruption of C/EBPα Function in Acute Myeloid Leukemia

In acute myeloid leukemia (AML), the most common type of acute leukemia in adults, there is clonal expansion and arrested maturation of myeloid precursor cells in the bone marrow, frequently resulting in granulocytopenia, thrombocytopenia, and anemia. The genetic abnormalities underlying these events fall into distinct classes. One class arises from mutations that affect lineage-specific transcription factors involved in hematopoietic-cell differentiation.1,2 These mutations, which disrupt cellular differentiation, are crucial events in the pathogenesis of a subgroup of cases of AML. Another class of genetic events comprises mutations that affect intracellular signaling molecules in a way that enhances cell proliferation and . . .