
FMS‐Like Tyrosine Kinase 3 in Normal Hematopoiesis and Acute Myeloid Leukemia
Author(s) -
Parcells Bertrand W.,
Ikeda Alan K.,
SimmsWaldrip Tiffany,
Moore Theodore B.,
Sakamoto Kathleen M.
Publication year - 2006
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1634/stemcells.2005-0519
Subject(s) - biology , myeloid leukemia , haematopoiesis , tyrosine kinase , myeloid , cancer research , leukemia , cd135 , stem cell , immunology , microbiology and biotechnology , signal transduction
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.