Maintenance therapy for <i>FLT3-ITD</i>-mutated acute myeloid leukemia
Andreas Burchert
Abstract
FLT3-ITD is a constitutively activated variant of the FLT3 tyrosine kinase receptor. Its expression in acute myeloid leukemia (AML) is associated with a poor prognosis. Due to this, the development of tyrosine kinase inhibitors (TKI) blocking FLT3-ITD became a rational therapeutic concept. This review describes key milestones in the clinical development of different FLT3-specific TKI with a particular focus on FLT3-TKI maintenance therapy in remission after allogeneic hematopoietic stem cell transplantation (HCT). Recent evidence from randomized trials using sorafenib in FLT3-ITD mutated AML provided a proof of concept that targeted post-HCT maintenance therapy could become a new treatment paradigm in AML.
Topics & Concepts
SorafenibMyeloid leukemiaMedicineFms-Like Tyrosine Kinase 3Tyrosine kinaseTargeted therapyOncologyHaematopoiesisCD135Tyrosine-kinase inhibitorMyeloidInternal medicineCancer researchLeukemiaClinical trialMaintenance therapyStem cellReceptorBiologyMutationChemotherapyCancerBiochemistryGeneGeneticsHepatocellular carcinomaAcute Myeloid Leukemia ResearchChronic Myeloid Leukemia TreatmentsHematopoietic Stem Cell Transplantation