| Literature DB >> 33472354 |
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.Entities:
Year: 2021 PMID: 33472354 PMCID: PMC7927878 DOI: 10.3324/haematol.2019.240747
Source DB: PubMed Journal: Haematologica ISSN: 0390-6078 Impact factor: 9.941