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Mutations in FLT3 receptor tyrosine kinase are the most frequently identified genetic event in acute myeloid leukemia (AML) that results in constitutive activation of survival and proliferation pathways including JAK/STAT, PI3K and RAS/MAPK pathways. The two major activating mutations in FLT3 gene are the internal tandem duplications (ITDs) of the juxtamembrane domain and the activation loop mutations of the tyrosine kinase domain . Thus, tyrosine kinases such as FLT3 represent an attractive therapeutic target for cancer therapies in AML. Several FLT3 tyrosine kinase inhibitors (TKIs) are currently under investigation including PKC-412.
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