Stromal Neoplasm

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT P551_E554delPMYE primary activating mutation demonstrated sensitivity to ponatinib treatment (IC50: 15nM). IC50 was determined b… (full text at CIViC)

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

In a prospective study of 137 gastrointestinal stromal tumor patients who failed imatinib treatment, tumors with KIT exon 11 mutations (52/89) treated with sunitinib were associated with shorter prog… (full text at CIViC)

PMID 22439647 · Rutkowski et al., 2012 · 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

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

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT P551_E554delPMYE primary activating mutation demonstrated insensitivity to regorafenib (IC50: 141nmol/L), imatinib (IC50: 90nmol… (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

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, 29 gastrointestinal stromal tumors with morphologic diagnosis by H&E staining and immunoreactivity to KIT (CD117) were evaluated for gain of function KIT or PDGFRA variants. … (full text at CIViC)

PMID 19943934 · Ostrowski et al., 2009 · Open in CIViC

In a retrospective study, a Chinese gastrointestinal stromal tumor patient harboring KIT Q556_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

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 16551858 · Wardelmann et al., 2006 · Open in CIViC

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 22089421 · Corless et al., 2011 · Open in CIViC

Gastrointestinal stromal tumor (GIST) patients with exon 9 mutations in KIT were less likely to show a complete or partial response to imatinib (44.4% vs. 71.7%, P=0.007) and had a shorter time to tum… (full text at CIViC)

PMID 20008851 · Gramza et al., 2009 · Open in CIViC

Gastrointestinal stromal tumor (GIST) patients with exon 9 mutations in KIT were less likely to show a complete or partial response to imatinib (44.4% vs. 71.7%, P=0.007) and had a shorter time to tum… (full text at CIViC)

PMID 16624552 · Debiec-Rychter et al., 2006 · Open in CIViC

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 16551858 · Wardelmann et al., 2006 · Open in CIViC

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 22089421 · Corless et al., 2011 · Open in CIViC

This patient was part of a larger cohort of 397 patients with incurable (i.e. metastatic or unresectable) CD117-positive Gastrointestinal stromal tumors (GISTs) enrolled in the North American phase II… (full text at CIViC)

PMID 18955451 · Heinrich et al., 2008 · Open in CIViC

In an in vitro study, a 32D cell line expressing KIT T417_D419del>I mutation (overexpression) demonstrated increased sensitivity to sunitinib treatment (IC50: 7.4nM) similar to 32D cells expressing KI… (full text at CIViC)

PMID 24205792 · Zhao 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

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 22089421 · Corless et al., 2011 · Open in CIViC

Primary KIT mutations are detected in 75-80% of GIST patients, and primarily occur in exons 9 and 11, wheareas secondary KIT mutations associated with resistance to imatinib are found in exons 13,14, … (full text at CIViC)

PMID 20043176 · Wang et al., 2010 · Open in CIViC

147 patients with advanced, unresectable GISTs were enrolled onto a randomized, phase II clinical study of imatinib (CSTI571-B2222). Specimens from 43 pretreatment and/or imatinib-resistant tumors wer… (full text at CIViC)

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

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