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Article

Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).

Blood - 1 Jan 2005

Kindler Thomas, Breitenbuecher Frank, Kasper Stefan, Estey Eli, Giles Francis, Feldman Eric, Ehninger Gerhard, Schiller Gary, Klimek Virginia, Nimer Stephen D, Gratwohl Alois, Choudhary Chuna Ram, Mueller-Tidow Constan, Serve Hubert, Gschaidmeier Harald, Cohen Pamela S, Huber Christoph, Fischer Thomas

Abstract excerpt

Fms-like tyrosine kinase 3 (FLT3) receptor mutations as internal tandem duplication (ITD) or within the kinase domain are detected in up to 35% of patients with acute myeloid leukemia (AML). N-benzoyl staurosporine (PKC412), a highly effective inhibitor of mutated FLT3 receptors, has significant...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 15345593
DOI: 10.1182/blood-2004-02-0660

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-15345593-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).PMID 15345593Read ↗

Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML.Semantic proximity Read ↗

Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.Semantic proximity Read ↗

Structural and functional alterations of FLT3 in acute myeloid leukemia.Semantic proximity Read ↗

Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation.Semantic proximity Read ↗

Tyrosine 842 in the activation loop is required for full transformation by the oncogenic mutant FLT3-ITD.Semantic proximity Read ↗

FLT3 mutations: biology and treatment.Semantic proximity Read ↗

FLT3 as a therapeutic target in AML: still challenging after all these yearsSemantic proximity Read ↗

Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412.Semantic proximity Read ↗

Activating FLT3 mutants show distinct gain-of-function phenotypes in vitro and a characteristic signaling pathway profile associated with prognosis in acute myeloid leukemia.Semantic proximity Read ↗

Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domainSemantic proximity Read ↗

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

Sensitivity toward tyrosine kinase inhibitors varies between different activating mutations of the FLT3 receptorSemantic proximity Read ↗

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