title: FMS-like tyrosine kinase 3 in normal hematopoiesis and acute myeloid leukemia.
abstract: Ligand-mediated activation of the FMS-like tyrosine kinase 3 (FLT3) receptor is important for normal proliferation of primitive hematopoietic cells. However, activating mutations in FLT3 induce ligand-independent downstream signaling that promotes oncogenesis through pathways involved in proliferation, differentiation, and survival. FLT3 mutations are identified as the most frequent genetic abnormality in acute myeloid leukemia and are also observed in other leukemias. Multiple small-molecule inhibitors are under development to target aberrant FLT3 activity that confers a poor prognosis in patients.
authors.affiliation: Division of Hematology-Oncology, Department of Pediatrics, Mattel Children's Hospital, Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA.
authors.forename: Bertrand W
authors.initials: BW
authors.lastname: Parcells
authors.forename: Alan K
authors.initials: AK
authors.lastname: Ikeda
authors.forename: Tiffany
authors.initials: T
authors.lastname: Simms-Waldrip
authors.forename: Theodore B
authors.initials: TB
authors.lastname: Moore
authors.forename: Kathleen M
authors.initials: KM
authors.lastname: Sakamoto
mesh_terms: D002986:Clinical Trials as Topic; D006410:Hematopoiesis; D006801:Humans; D015479:Leukemia, Myelomonocytic, Acute / Q000201:enzymology* / Q000235:genetics*; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D015398:Signal Transduction; D051941:fms-Like Tyrosine Kinase 3 / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism
chemical_list: D047428:Protein Kinase Inhibitors; D051941:fms-Like Tyrosine Kinase 3