Activated FLT3 Receptor Tyrosine Kinase as a Therapeutic Target In Leukemia

摘要: Acute myeloid leukemia (AML) is a heterogeneous neoplastic disease characterized by deregulated proliferation of precursor cells combined with an arrest in the differentiation process. The abnormal survival advantage transformed immature precursors further contributes to marked impairment functional maturation various cell lineages. Intensive studies over past 20 yr have resulted identification leukemia-specific cytogenetic abnormalities, which provided considerable insight into underlying pathogenesis AML. This has also prognostic stratification AML patients three different risk groups: those favorable, intermediate or standard, and poor disease. Patients favorable cytogenetics, i.e., translocations t(15;17), t(8;21), inversion inv(16), particularly benefited from improved understanding molecular pathology their disease, potential therapeutic targets. For example, addition all-trans retinoic acid during induction chemotherapy for acute promyelocytic (APL) PML/RARα (promyelocytic leukemia/retinoic receptor-α) fusion gene t(15;17) increased 5-yr 20–30% compared alone (1,2).