FMS-Like Tyrosine Kinase 3 in Normal Hematopoiesis and Acute Myeloid Leukemia

2006/01/12 by Bertrand W. Parcells, Alan K. Ikeda, Tiffany Simms-Waldrip +2
Medicine · #Acute Myeloid Leukemia Research #Chronic Lymphocytic Leukemia Research #Chronic Myeloid Leukemia Treatments

paper · pdf · doi:10.1634/stemcells.2005-0519

openalex publication_date 2006/01/12 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29

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.

Related

• FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications
• Targeting FLT3 mutations in AML: review of current knowledge and evidence
• The role of FLT 3 inhibitors in the treatment of FLT 3‐mutated acute myeloid leukemia
• Evolving paradigms in targeting FLT3 for acute myeloid leukemia therapy
• Selective targeting of RSK signaling with PMD-026 suppresses FLT3-activated acute myeloid leukemia while sparing normal hematopoiesis