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Open Access Green as soon as Postprint is submitted to ZB.
A new and recurrent activating length mutation in exon 20 of the FLT3 gene in acute myeloid leukemia.
Blood 100, 3423-3425 (2002)
Activating length mutations in the juxtamembrane (JM) domain of the FLT3 gene (FLT3-LM) and mutations in the catalytic domain (FLT3D835/836) of this receptor tyrosine kinase represent the most frequent genetic alterations in acute myeloid leukemia (AML). Here, we describe a 6-bp insertion in the activation loop of FLT3 between codons 840 and 841 of FLT3 (FLT3-840GS) in 2 unrelated patients with AML. Screening for other activating mutations of FLT3, KIT, and NRASshowed no further genetic alterations in patients carrying the FLT3-840GS. In functional analyses we could show that this mutant is hyperphosphorylated on tyrosine and confers interleukin 3–independent growth to Ba/F3 cells, which can be inhibited by a specific FLT3 protein tyrosine kinase (PTK) inhibitor. Our results show for the first time that in addition to known mutations in the JM and the catalytic domain, further activating length mutations exist in theFLT3 gene.
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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0006-4971
e-ISSN
1528-0020
Journal
Blood
Quellenangaben
Volume: 100,
Pages: 3423-3425
Publisher
American Society of Hematology
Reviewing status
Peer reviewed
Institute(s)
CCG Pathogenesis of Acute Myeloid Leukemia (KKG-KPL)