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  • Acute myelogenous leukemia (AML) is a malignancy originating in a multipotential hematopoietic cell characterized by clonal proliferation of abnormal blast cells in the marrow and impaired production of normal blood cells, resulting in anemia; thrombocytopenia; and low, normal, or high white cell counts depending on the number of leukemic cells in the blood. It occurs in nine morphologic variants, each with characteristic cytologic, genetic, and sometimes clinical features.


  • The chronic clonal myeloid diseases may progress to florid AML (e.g., polycythemia vera, Chap. 43; essential thrombocythemia, Chap. 44), clonal cytopenias, Chap. 42; chronic myelogenous leukemia, Chap. 47).

  • AML may develop with increased frequency in patients with certain congenital (Down syndrome) or inherited abnormalities (e.g., Fanconi anemia, familial platelet syndrome) as shown in Table 46–1.

  • Non-syndromic, familial occurrence, suggesting an inherited predisposition gene, has been documented but is uncommon.

  • Most cases arise de novo and are associated with acquired cytogenetic changes, including translocation, inversions, deletions, and others. These changes lead to the mutation of protooncogenes and the formation of oncogenes. Frequently, the latter encode mutant transcription factors that result in disruption of cell signaling pathways that cause malignant transformation.

  • AML results from a series of somatic mutations in a multipotential hematopoietic cell or, in a small proportion of cases, a more differentiated, lineage restricted progenitor cell. In acute promyelocytic leukemia (APL), some cases of monocytic leukemia, and some young persons with other forms of AML, the disease originates in a mutated granulocytic-monocytic progenitor cell.

  • AML requires at least two types of mutation: a primary oncogenic mutation, such as involving core-binding factor subunit genes (CBF-β or RUNX1), and an activating mutation, in a hematopoietic tyrosine kinase, such as FMS-like tyrosine kinase 3 (FLT3). The mutations in AML result in deregulated signaling pathways that disrupt differentiation and maturation, regulation of proliferation and of cell survival in varying combinations.




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