Abstract

Acute myeloid leukemia (AML) is a heterogeneous group of clonal malignant myeloid neoplasms. Malignant transformation of hematopoietic progenitor cell leads to clonal expansion and replacement of normal bone marrow cells with malignant cells leading to suppression of normal haematopoiesis. Advancements in our understanding of disease biology have allowed AML to be classified based on its gene expression profile, which includes previously identified cytogenetic subgroups, and distinct novel subgroups which have prognostic significance. Identification of mutations in DNMT3A and IDH 1 genes in cytogenetically normal AML (by gene sequencing) helps to identify patients with poor prognosis. Redesigning the treatment regimen consisting of cytarabine and daunorubicin has improved the treatment outcomes without increase in the treatment-related mortality. Increasing the dose of daunorubicin to 90 mg/m 2 improves complete remission rates without increasing treatment-related complications both in young and elderly patients. Cytarabine (200 mg/m 2 in cycle I and 2 g/m 2 in cycle 2) is shown to be as effective as high dose cytarabine (1000 mg/m 2 twice daily in cycle 1and 2 g/m 2 twice daily in cycle 2) and is associated with less treatment-related toxicities.

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