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Article

The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.

Blood - 15 Feb 2003

Spiekermann Karsten, Dirschinger Ralf J, Schwab Ruth, Bagrintseva Ksenia, Faber Florian, Buske Christian, Schnittger Susanne, Kelly Louise M, Gilliland D Gary, Hiddemann Wolfgang

Abstract excerpt

Activating mutations of the protein tyrosine kinase (PTK) FLT3 can be found in approximately 30% of patients with acute myeloid leukemia (AML), thereby representing the most frequent single genetic alteration in AML. These mutations occur in the juxtamembrane (FLT3 length mutations; FLT3-LMs) and the second tyrosine kinase domain of FLT3-TKD and confer interleukin 3 (IL-3)-independent growth to Ba/F3 cells. In...

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Source

Identifiers

PMID: 12406902
DOI: 10.1182/blood-2002-04-1045

Genes

FLT3

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3.PMID 12406902Read ↗

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Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AMLSemantic proximity Read ↗

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