Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Molecular cancer therapeutics - 1 Oct 2002

Frost Michelle J, Ferrao Petranel T, Hughes Timothy P, Ashman Leonie K

Abstract excerpt

Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor. Overexpression or constitutive activation of Kit by mutations have been associated with various malignancies. Mutations in the intracellular juxtamembrane region of Kit (e.g., V560G) are common in gastrointestinal stromal tumors and have been linked to poor prognosis. Mutations...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Annexin A5
Share to Benzamides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Granulocyte-Macrophage Colony-Stimulating Factor

Share to Imatinib Mesylate

Share to Piperazines

Share to Precipitin Tests

Share to Retroviridae

Share to STAT3 Transcription Factor

Source

Identifiers

PMID: 12481435

Genes

STAT3
BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant.PMID 12481435Read ↗

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

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

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

Targeting c-kit mutations in solid tumors: scientific rationale and novel therapeutic options.Semantic proximity Read ↗

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

Constitutive activation of c-kit by the juxtamembrane but not the catalytic domain mutations is inhibited selectively by tyrosine kinase inhibitors STI571 and AG1296.Semantic proximity Read ↗

Pharmaco-phosphoproteomic analysis of cancer-associated KIT mutations D816V and V560G.Semantic proximity Read ↗

STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications.Semantic proximity Read ↗

Direct engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.Semantic proximity Read ↗

A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient.Semantic proximity Read ↗

Imatinib inhibits various types of activating mutant kit found in gastrointestinal stromal tumors.Semantic proximity Read ↗

[Therapeutically relevant mutations in the receptor tyrosine kinase KIT in mastocytosis].Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.