Connective and Soft Tissue Neoplasm

The GIST882 patient derived cell line expressing KIT K642E mutation demonstrated sensitivity to ponatinib (IC50: 31nmol/L) and sunitinib (IC50: 54nmol/L) treatments. In comparison, the insensitve KIT-… (full text at CIViC)

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

A cell line derived from GIST882 patients expressing KIT K642E mutation demonstrated insensitivity to regorafenib (IC50: 503nmol/L) treatment. IC50 was determined by assessing cell viability.

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

In an in vitro study, a GIST 882 cell line expressing KIT K642E mutation demonstrated increased sensitivity to regorafenib treatment (IC50: 45 nM vs. 560-3269nM) compared to HepG2, SW620, Colo-205 or … (full text at CIViC)

PMID 21170960 · Wilhelm et al., 2011 · Open in CIViC

In an in vitro study, GIST882 cells expressing KIT K642E mutation (endogenous expression) demonstrated sensitivity to sunitinib treatment (IC50<50nM). Sensitivity was determined by assessing KIT auto-… (full text at CIViC)

PMID 16638875 · Prenen et al., 2006 · Open in CIViC

The variant observed in GIST gene coding region c.1925A>G leads to protein change of p.K642R .This variant is observed in asian GIST patients.

PMID 28975118 · Pai et al., 2017 · 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 29 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 L576P mutati… (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 this phase II, randomized, open-label trial, 147 patients with histologically confirmed, unresectable or metastatic gastrointestinal stromal tumour that expressed CD117 were enrolled. Patients were… (full text at CIViC)

PMID 12181401 · Demetri et al., 2002 · Open in CIViC

Human GISTs with different KIT mutations were grafted in 136 nude muce. Mice were then treated with control, imatinib, GDC-0941, or GDC-0941 + imatinib. The combination showed superior antitumor effic… (full text at CIViC)

PMID 23231951 · Floris et al., 2013 · 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

Ponatinib possesses potent activity against N882K KIT mutant in preclinical experiments.

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

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

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