Abstract

Background Internal tandem duplication (ITD) mutations in the juxtamembrane domain–coding sequence of the Fms-like tyrosine kinase 3 ( FLT3 ) gene have been identified in 30% of acute myeloid leukemia (AML) patients and are associated with a poor prognosis. The kinase inhibitor sorafenib induces growth arrest and apoptosis at much lower concentrations in AML cell lines that harbor FLT3-ITD mutations than in AML cell lines with wild-type FLT3.