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Acute myelogenous leukemia (AML) is the result of a sequence of somatic mutations in a primitive multipotential hematopoietic cell. Exposure to radiation, chronic exposure to high doses of benzene, and chronic inhalation of tobacco smoke increase the incidence of the disease. Obesity is also an endogenous risk factor. A small but increasing proportion of cases develop after a patient with lymphoma, a nonhematologic cancer, or an autoimmune disorder is exposed to intensive chemotherapy, especially with alkylating agents platinum derivatives, or topoisomerase II inhibitors. The mutant (leukemic) hematopoietic cell is capable of self-renewal and desultory differentiation and maturation. It gains a growth and survival advantage in relationship to the normal polyclonal pool of HSCs. As the progeny of this mutant, now leukemic, multipotential cell proliferates to form approximately 10–100 billion or more cells, normal hematopoiesis is inhibited, and normal red cell, neutrophil, monocyte, and platelet blood counts fall. The resultant anemia leads to weakness, exertional limitations, and pallor; the neutropenia and monocytopenia leads to poor wound healing and minor infections; and the thrombocytopenia leads to spontaneous hemorrhage, usually in the skin and mucous membranes. Severe infection usually does not occur at diagnosis, but often does if the disease progresses because of lack of treatment or if chemotherapy intensifies the decrease of blood neutrophil and monocyte levels. The diagnosis is made by measurement of blood cell counts and examination of blood and marrow cells and is based on identification of leukemic blast cells in the blood and marrow. The diagnosis of the myelogenous form of acute leukemia is confirmed specifically by identification of myeloperoxidase activity in blast cells or by identifying characteristic cluster of differentiation (CD) antigens on the blast cells (eg, CD13, CD33). Because the leukemic stem cell is capable of imperfect differentiation and maturation, the clone may contain cells that have the morphologic or immunophenotypic features of erythroblasts, megakaryocytes, monocytes, eosinophils, or, rarely, basophils or mast cells, in addition to myeloblasts or promyelocytes. When one cell line is sufficiently dominant, the leukemia may be referred to by that lineage, for example, acute erythroid, acute megakaryocytic, acute monocytic leukemia. Certain cytogenetic alterations are more frequent; these abnormalities include t(8;21), t(15;17), inversion 16 or t(16;16), trisomy 8, and deletions of all or part of chromosome 5 or 7. A translocation involving chromosome 17 at the site of the retinoic acid receptor-α (RARα) gene is uniquely associated with acute promyelocytic leukemia. Some AML cases are associated with recurrent somatic mutations that can be targeted therapeutically. AML usually is treated with cytarabine and an anthracycline, although other drugs may be added or substituted in patients with poor prognosis or who are refractory, relapsed, or older, or in patients with specific somatic mutations (eg, FLT3, IDH1, or IDH2) for which new drugs have been developed. The exception to this approach is the treatment of acute promyelocytic leukemia with all-trans retinoic acid, arsenic trioxide, and sometimes an anthracycline. High-dose chemotherapy and either ...

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