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Acute myelogenous leukemia (AML) is the result of a sequence of somatic mutations in a multipotential primitive hematopoietic cell or, in some cases, a more differentiated progenitor cell. Exposure to radiation, chronic exposure to high doses of benzene, and chronic, heavy inhalation of tobacco smoke increase the incidence of the disease. A small but increasing proportion of cases develop after a patient with lymphoma or a nonhematologic cancer is exposed to intensive chemotherapy, especially with alkylating agents or topoisomerase II inhibitors. The mutant hematopoietic cell gains a growth and/or survival advantage in relationship to the normal pool of stem cells. As the progeny of this mutant, now leukemic, multipotential cell proliferates to form approximately 11 billion or more cells, normal hematopoiesis is inhibited, and normal red cell, neutrophil, and platelet blood levels fall. The resultant anemia leads to weakness, exertional limitations, and pallor; the thrombocytopenia to spontaneous hemorrhage, usually in the skin; and the neutropenia and monocytopenia to poor wound healing and minor infections. Severe infection usually does not occur at diagnosis but will 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 marrow and blood. The diagnosis of AML specifically is confirmed by identification of myeloperoxidase activity in blast cells or by identifying characteristic cluster of differentiation (CD) antigens on the blast cells (e.g., CD13, CD33). 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 as acute erythroid, acute megakaryocytic, acute monocytic, and so on. Certain cytogenetic alterations are more frequent and include t(8;21), t(15;17), inversion 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 alpha (RAR-α) gene is uniquely associated with acute promyelocytic leukemia. AML usually is treated with cytarabine and an anthracycline antibiotic, although other drugs may be added or substituted in poor-prognosis, refractory, or relapsed patients. The exception to this approach is the treatment of acute promyelocytic leukemia with all-trans-retinoic acid, arsenic trioxide, and an anthracycline antibiotic. High-dose chemotherapy and either autologous stem cell infusion or allogeneic stem cell transplantation may be used in an effort to treat relapse or patients at high risk to relapse after chemotherapy treatment. The probability of remission ranges from approximately 80 percent in children to less than 25 percent in octogenarians. The probability for cure decreases from approximately 50 percent in children to virtually zero in octogenarians.

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