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C/EBPα and the pathophysiology of acute myeloid leukemia

Purpose of reviewThe transcription factor C/EBPα controls differentiation and proliferation in normal granulopoiesis in a stage-specific manner. Loss of C/EBPα function in myeloid cells in vitro and in vivo leads to a block to myeloid differentiation similar to that which is observed in malignant cells from patients with acute myeloid leukemia. The finding of C/EBPα alterations in subgroups of acute myeloid leukemia patients suggests a direct link between critically decreased C/EBPα function and the development of the disorder. Recent findingsConditional mouse models provide direct evidence that loss of C/EBPα function leads to the accumulation of myeloid blasts in the bone marrow. Targeted disruption of the wild type C/EBPα protein, while conserving the dominant-negative 30 kDa isoform of C/EBPα, induces an AML-like disease in mice. In hematopoietic stem cells C/EBPα serves to limit cell self-renewal. Finally, C/EBPα function is disrupted at different levels in specific subgroups of acute myeloid leukemia patients. SummaryThere is evidence that impaired C/EBPα function contributes directly to the development of acute myeloid leukemia. Normal myeloid development and acute myeloid leukemia are now thought to reflect opposite sides of the same hematopoietic coin. Restoring C/EBPα function represents a promising target for novel therapeutic strategies in acute myeloid leukemia.