Mesenchymal Cell Neoplasm

A preclinical study tested the effects of a tyrosine kinase inhibitor (TKI) on Ba/F3 cell lines with representative primary regorafenib-sensitizing mutation del 557-558, which induced IL-3 independent… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

Several preclinical studies tested the effects of various tyrosine kinase inhibitors (TKIs) on Ba/F3 cell lines with representative primary sunitinib-sensitizing mutation del 557-558 and secondary mut… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

In a retrospective study, a Chinese gastrointestinal stromal tumor patient harboring KIT V555_I571del deletion mutation was associated with improved response to sunitinib treatment after failed imatin… (full text at CIViC)

PMID 23456621 · Gao et al., 2013 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

Patient 36 from a larger cohort of genotyped patients (n= 78) with imatinib resistant or intolerant gastrointestinal stromal tumors (GISTs) harbored a primary (pre-imatinib treatment) KIT V555_V559 de… (full text at CIViC)

PMID 18955458 · Heinrich et al., 2008 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

A novel compound identified in a high-throughput screen is highly selective for KIT V559D in cell lines and mice models. In mice, there was a dose-dependent reduction in tumor size.

PMID 29340041 · Yu et al., 2017 · Open in CIViC

dasatinib inhibited cell growth of imatinib-sensitive KIT V559D with an IC50 of 27 nmol/L, whereas imatinib, nilotinib, and sorafenib had an IC50 of 63, 44, and 66 nmol/L, respectively.

PMID 17699867 · Guo et al., 2007 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In a retrospective study of 1124 sunitinib-treated gastrointestinal stromal tumor patients, patients with primary KIT exon 11 mutations (n=143) were associated with decreased progression free surviva… (full text at CIViC)

PMID 26772734 · Reichardt et al., 2016 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In a retrospective study of 123 metastatic or advanced gastrointestinal stromal tumor patients with KIT exon 11 mutations, patients with KIT exon 11 mutations were reported to be responsive to sunitin… (full text at CIViC)

PMID 26416414 · Vincenzi et al., 2016 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT V560D primary activating mutation demonstrated sensitivity to imatinib (IC50: 3nmol/L), sunitinib (IC50: 2nmol/L), regorafenib (… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In a phase 1/2 trial of 97 gastrointestinal stromal tumor patients, patients with KIT exon 11 mutations (44/77) treated with sunitinib were associated with shorter progression free survival (5.1mo vs.… (full text at CIViC)

PMID 18955458 · Heinrich et al., 2008 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In the patient-derived cell line GIST430 harboring KIT V560_L576del primary activating mutation implanted in mice, imatinib and ponatinib were shown to reduce KIT phosphorylation compared to the vehic… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

A GIST430 patient derived cell line expressing KIT V560_L576del primary activating mutation demonstrated insensitivity to regorafenib (IC50: 191nmol/L) treatment. IC50 was determined by assessing cell… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

In a phase 1/2 trial of 97 gastrointestinal stromal tumor patients, patients with KIT exon 11 mutations (44/77) treated with sunitinib were associated with shorter progression free survival (5.1mo vs.… (full text at CIViC)

PMID 18955458 · Heinrich et al., 2008 · Open in CIViC

KIT V654A results in imatinib resistance in GIST patient-derived cell lines.

PMID 16954519 · Heinrich et al., 2006 · Open in CIViC

In an in vitro study, Ba/F3 cell lines expressing different KIT primary mutations (known to confer sensitivity to regorafenib) and KIT V654A secondary mutation, KIT V654A was associated with decreased… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In a phase 1/2 trial of 97 gastrointestinal stromal tumor patients, patients with KIT exon 11 mutations (44/77) treated with sunitinib were associated with shorter progression free survival (5.1mo vs.… (full text at CIViC)

PMID 18955458 · Heinrich et al., 2008 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In a retrospective study of 1124 sunitinib-treated gastrointestinal stromal tumor patients, patients with primary KIT exon 11 mutations (n=143) were associated with decreased progression free surviva… (full text at CIViC)

PMID 26772734 · Reichardt et al., 2016 · Open in CIViC

Molecular models predict that deletion of a portion of the juxtamembrane domain relieves steric hindrance and results in higher binding affinity for imatinib.

PMID 21364689 · Pierotti et al., 2011 · Open in CIViC

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT W557_K558del primary activating mutation demonstrated sensitivity to imatinib (IC50: 27nmol/L) and ponatinib (IC50: 3nmol/L) tre… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · Open in CIViC