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

Functional analyses and molecular modeling of two c-Kit mutations responsible for imatinib secondary resistance in GIST patients.

Oncogene - 5 Oct 2006

Tamborini E, Pricl S, Negri T, Lagonigro M S, Miselli F, Greco A, Gronchi A, Casali P G, Ferrone M, Fermeglia M, Carbone A, Pierotti M A, Pilotti S

Abstract excerpt

Imatinib-acquired resistance related to the presence of secondary point mutations has become a frequent event in gastrointestinal stromal tumors. Here, transient transfection experiments with plasmids carrying two different KIT-acquired point mutations were performed along with immunoprecipitation of total protein extracts, derived from imatinib-treated and untreated cells. The molecular mechanics/Poisson...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Agents
Share to Benzamides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Gastrointestinal Stromal Tumors

Share to Imatinib Mesylate

Share to Piperazines

Share to Proto-Oncogene Proteins c-kit

Share to Pyrimidines

Source

Identifiers

PMID: 16751810
DOI: 10.1038/sj.onc.1209639

Genes

KIT

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

Functional analyses and molecular modeling of two c-Kit mutations responsible for imatinib secondary resistance in GIST patients.PMID 16751810Read ↗

Are two better than one? A novel double-mutant KIT in GIST that responds to Imatinib.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 ↗

Activate and resist: L576P-KIT in GIST.Semantic proximity Read ↗

Insight on Mutation-Induced Resistance from Molecular Dynamics Simulations of the Native and Mutated CSF-1R and KIT.Semantic proximity Read ↗

Lessons from Structural Biology for Understanding Drug Resistance in Gastrointestinal Stromal Tumors (GIST).Semantic proximity Read ↗

T670X KIT Mutations in Gastrointestinal Stromal Tumors: Making Sense of MissenseSemantic proximity Read ↗

Differential effects of CSF-1R D802V and KIT D816V homologous mutations on receptor tertiary structure and allosteric communication.Semantic proximity Read ↗

KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients.Semantic proximity Read ↗

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

Hotspot mutations in KIT receptor differentially modulate its allosterically coupled conformational dynamics: impact on activation and drug sensitivity.Semantic proximity Read ↗

A shift of dynamic equilibrium between the KIT active and inactive states causes drug resistance.Semantic proximity Read ↗

Mutation D816V alters the internal structure and dynamics of c-KIT receptor cytoplasmic region: implications for dimerization and activation mechanisms.Semantic proximity Read ↗

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