FMS-like tyrosine kinase 3 in normal hematopoiesis and acute myeloid leukemia

Bertrand W. Parcells, Alan K. Ikeda, Tiffany Simms-Waldrip, Theodore B. Moore, Kathleen M. Sakamoto

Research output: Contribution to journalReview article

71 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1174-1184
Number of pages11
JournalSTEM CELLS
Volume24
Issue number5
DOIs
StatePublished - May 1 2006

Keywords

  • Acute myeloid leukemia
  • FMS-like tyrosine kinase 3
  • Hematopoiesis
  • Internal tandem duplication
  • Small molecule inhibitor

ASJC Scopus subject areas

  • Molecular Medicine
  • Developmental Biology
  • Cell Biology

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