[Molecular mechanisms in the development of acute myeloid leukemia]

Acute myeloid leukemia (AML) is a malignant hematopoietic neoplasm characterized by clonal proliferation of tumor cells that arise from the hematopoietic stem/progenitor population within the bone marrow. Cytogenetic abnormalities or point mutations of the hematopoiesis-specific genes are frequently found in patients with AML, and these genetic aberrations are closely associated with the pathophysiology of the disease. Molecular pathogenesis of AML has been disclosed through analyses of such gene aberrations, including AML1 and MLL abnormalities, PML-RARA chimeric gene, activating mutations of FLT3, and EVI-1 abnormalities. Through prediction of prognosis and targeted therapy, this knowledge on pathogenesis of AML has been applied to the clinical practice, and further investigation should improve the outcome of therapy for AML in the future.