Perspectives and challenges of small molecule inhibitor therapy for FLT3-mutated acute myeloid leukemia.

Abstract excerpt

Acute myeloid leukemia (AML) is a heterogeneous clonal disease characterized overall by an aggressive clinical course. The underlying genetic abnormalities present in leukemic cells contribute significantly to the AML phenotype. Mutations in FMS-like tyrosine kinase 3 (FLT3) are one of the most common genetic abnormalities identified in AML, and the presence of these mutations strongly influences disease...

Topics

• fms-Like Tyrosine Kinase 3
• Humans
• Leukemia, Myeloid, Acute
• Mutation
• Protein Kinase Inhibitors
• Antineoplastic Agents