FMS-like tyrosine kinase 3 in normal hematopoiesis and acute myeloid leukemia.
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.
Parcells
Bertrand W
BW
Division of Hematology-Oncology, Department of Pediatrics, Mattel Children's Hospital, Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA.
Ikeda
Alan K
AK
Simms-Waldrip
Tiffany
T
Moore
Theodore B
TB
Sakamoto
Kathleen M
KM
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
D047428:Protein Kinase Inhibitors; D051941:fms-Like Tyrosine Kinase 3