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Abstract Acute myeloid leukemia (AML) is a heterogeneous group of disorders that can be discriminated by morphology, immunophenotyping or more recently by cytogenetic and molecular techniques (Hiddemann et al., 2003). Acute myeloid leukemia (AML) is a malignant neoplasm of hematopoietic cells characterized by an abnormal proliferation of myeloid precursor cells, decreased rate of self-destruction and an arrest in cellular differentiation. The leukemic cells have an abnormal survival advantage. Thus, the bone marrow and peripheral blood are characterized by leukocytosis with a predominance of immature cells, primarily blasts (McKenzie., 2005). As the immature cells accumulate in the bone marrow, they replace the normal myelocytic cells, megakaryocytes, and erythrocytic cells. This leads to a loss of normal bone marrow function and associated complications of bleeding, anemia, and infection (McKenzie., 2005). Acute myeloid leukemia (AML) has an incidence of 2-3 per 100 000 per annum in children, rising to 15 per 100 000 in older adults. It can occur at all ages but has its peak incidence in the seventh decade (Burnett., 2005). |