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First published online January 12, 2006
Stem Cells Vol. 24 No. 5 May 2006, pp. 1174 -1184
doi:10.1634/stemcells.2005-0519; www.StemCells.com
© 2006 AlphaMed Press

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TRANSLATIONAL AND CLINICAL RESEARCH: CONCISE REVIEW

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

Bertrand W. Parcellsa, Alan K. Ikedaa, Tiffany Simms-Waldripa, Theodore B. Moorea, Kathleen M. Sakamotoa,b,c

a Division of Hematology/Oncology, Department of Pediatrics, Gwynne Hazen Cherry Memorial Laboratories, Mattel Children’s Hospital, Jonsson Comprehensive Cancer Center, Los Angeles, California, USA;
b Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA;
c Division of Biology, California Institute of Technology, Pasadena, California, USA

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

Correspondence: Kathleen M. Sakamoto, M.D., Ph.D., A2-412 MDCC CHS, Division of Hematology-Oncology, Mattel Children’s Hospital, David Geffen School of Medicine, UCLA, 10833 Le Conte Avenue, Los Angeles, California 90095-1752, USA. Telephone: 310-794-7007; Fax: 310-206-8089; e-mail: kms{at}ucla.edu, ksakamoto{at}mednet.ucla.edu

Received November 27, 2005; accepted for publication January 1, 2006.
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.




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