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

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

Molecular oncology - 1 Aug 2013

Conca Elena, Miranda Claudia, Dal Col Valentina, Fumagalli Elena, Pelosi Giuseppe, Mazzoni Mara, Fermeglia Maurizio, Laurini Erik, Pierotti Marco A, Pilotti Silvana, Greco Angela, Pricl Sabrina, Tamborini Elena

Abstract excerpt

Gastrointestinal stromal tumors carry in about 85% of the cases activating mutations in KIT gene. Generally only one KIT mutation is found in primary tumors and the majority of mutations affecting KIT exon 11 is sensitive to Imatinib. We report upon a GIST case harboring a double-mutant KIT gene...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Computational Biology
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gastrointestinal Stromal Tumors

Share to Imatinib Mesylate

Share to Piperazines

Share to Proto-Oncogene Proteins c-kit

Share to Pyrimidines

Source

Open in PubMed Open full text

Identifiers

PMID: 23567324
DOI: 10.1016/j.molonc.2013.02.019
PMCID: PMC5528426

Genes

KIT

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-23567324-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Are two better than one? A novel double-mutant KIT in GIST that responds to Imatinib.PMID 23567324Read ↗

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

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

p.(L576P) -KIT mutation in GIST: Favorable prognosis and sensitive to imatinib?Semantic proximity Read ↗

Virtual Screening and Molecular Docking: Discovering Novel c-KIT Inhibitors.Semantic proximity Read ↗

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

A holistic view on c-Kit in cancer: Structure, signaling, pathophysiology and its inhibitorsSemantic proximity Read ↗

CCR 20th Anniversary Commentary: A Genetic Mechanism of Imatinib Resistance in Gastrointestinal Stromal Tumor-Where Are We a Decade Later?Semantic proximity Read ↗

Structural and functional analysis of KIT gene encoding receptor tyrosine kinase and its interaction with sunitinib and HDAC inhibitors: an in silico approach.Semantic proximity Read ↗

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

Molecular mechanism of D816X mutation-induced c-Kit activation and -mediated inhibitor resistance in gastrointestinal stromal tumor.Semantic proximity Read ↗

The role of small molecule Kit protein-tyrosine kinase inhibitors in the treatment of neoplastic disorders.Semantic proximity Read ↗

Design of antitumor drugs targeting c-kit receptor by a new mixed ligand-structure based method.Semantic proximity Read ↗

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