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Article

Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412.

Blood - 15 Jul 2005

Growney Joseph D, Clark Jennifer J, Adelsperger Jennifer, Stone Richard, Fabbro Doriano, Griffin James D, Gilliland D Gary

Abstract excerpt

Constitutively activated forms of the transmembrane receptor tyrosine kinase c-KIT have been associated with systemic mast cell disease, acute myeloid leukemia, and gastrointestinal stromal tumors. Reports of the resistance of the kinase domain mutation D816V to the adenosine triphosphate (ATP)-competitive kinase inhibitor imatinib mesylate prompted us to characterize 14 c-KIT mutations reported in association...

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Source

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Identifiers

PMID: 15790786
DOI: 10.1182/blood-2004-12-4617
PMCID: PMC1895184

Genes

KIT

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412.PMID 15790786Read ↗

PKC412 inhibits in vitro growth of neoplastic human mast cells expressing the D816V-mutated variant of KIT: comparison with AMN107, imatinib, and cladribine (2CdA) and evaluation of cooperative drug effects.Semantic proximity Read ↗

Resistance to c-KIT kinase inhibitors conferred by V654A mutation.Semantic proximity Read ↗

Activity of the tyrosine kinase inhibitor PKC412 in a patient with mast cell leukemia with the D816V KIT mutation.Semantic proximity Read ↗

Juxtamembrane-type c-kit gene mutation found in aggressive systemic mastocytosis induces imatinib-resistant constitutive KIT activation.Semantic proximity Read ↗

Therapeutic targeting of c-KIT in cancer.Semantic proximity Read ↗

Mast cell disease associated with acute myeloid leukemia: detection of a new c-kit mutation Asp816His.Semantic proximity Read ↗

Tyrosine kinase inhibitors in the treatment of systemic mastocytosis.Semantic proximity Read ↗

Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant.Semantic proximity Read ↗

Mechanisms of resistance to imatinib mesylate in gastrointestinal stromal tumors and activity of the PKC412 inhibitor against imatinib-resistant mutants.Semantic proximity Read ↗

The c-Kit/D816V mutation eliminates the differences in signal transduction and biological responses between two isoforms of c-Kit.Semantic proximity Read ↗

KIT mutations in mastocytosis and their potential as therapeutic targets.Semantic proximity Read ↗

Mechanisms of STAT protein activation by oncogenic KIT mutants in neoplastic mast cells.Semantic proximity Read ↗

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