Abstract
FLT3, a tyrosine kinase receptor, is the most common mutation in AML and has two classes of mutations: internal tandem duplications in the juxtamembrane domain (FLT3-ITDs) and point mutations in the tyrosine kinase domain (FLT3-TKDs). AML patients with FLT3 mutations tend to have a poor prognosis. As an independent factor, the presences of FLT3 mutations play an important role in the origin and development of AML and have prognostic value. Molecular targeted therapy represents a novel and popular therapeutic approach in the world. In this review, we explain clinical value of the FLT3 mutations, mechanism and research progression of the FLT3 inhibitor;and discuss difficulties and perspectives in the research of the FLT3 inhibitor. Key words: Receptor protein-tyrosine kinases; Mutation; Inhibins; Leukemia,myelocytic,acute
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