Mesenchymal Cell Neoplasm

There is no significant association between wildtype KIT or KIT mutations in exon 9 or 11 in survival among GIST patients.

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

KIT mutations were identified in morphologically benign, incidentally discovered GISTs at a rate similar to that seen in advanced, metastatic GIST patients indicating is not a prognostic marker for GI… (full text at CIViC)

PMID 12000708 · Corless et al., 2002 · Open in CIViC

KIT mutation is associated with worse overall and cause-specific prognosis in patients with GIST compared to patients with wildtype KIT.

PMID 10485475 · Taniguchi et al., 1999 · Open in CIViC

KIT mutation is associated with larger, more invasive tumors, greater pathologic histology and older patients compared to tumors with wildtype KIT.

PMID 10485475 · Taniguchi et al., 1999 · Open in CIViC

This prospective study of 127 pretreatment patients with metastatic gastrointestinal stromal tumors (GISTs) examined the relationship between kinase (KIT and PDGFRA) genotype and treatment outcome for… (full text at CIViC)

PMID 14645423 · Heinrich et al., 2003 · Open in CIViC

This prospective study of 397 patients with incurable (i.e. metastatic or unresectable) CD117-positive Gastrointestinal stromal tumors (GISTs) examined the relationship between KIT genotype and treatm… (full text at CIViC)

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

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PMID 14645423 · Heinrich et al., 2003 · Open in CIViC

This phase II clinical trial of regorafenib (NCT01068769) examined the long term safety and efficacy of regorafenib in patients with metastatic and/or unresectable gastrointestinal stromal tumors (GIS… (full text at CIViC)

PMID 27371698 · Ben-Ami et al., 2016 · Open in CIViC

This international, placebo controlled prospective phase 3 clinical trial (NCT01271712) examined safety and efficacy of regorafenib in patients with metastatic and/or unresectable gastrointestinal str… (full text at CIViC)

PMID 23177515 · Demetri et al., 2013 · Open in CIViC

This retrospective study of a phase 2 clinical trial (NCT01068769) examined regorafenib safety and efficacy in advanced gastrointestinal stromal tumor (GIST) patients who failed previous treatments wi… (full text at CIViC)

PMID 22614970 · George et al., 2012 · Open in CIViC

In a phase I/II trial of sunitinib efficacy on imatinib resistant or intolerant gastrointestinal stromal tumor (GIST) patients (n=77), patients harboring primary (pre-imatinib treatment) KIT exon 11 m… (full text at CIViC)

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

This study describes a case report of a patient with a gastrointestinal stromal tumor who was prescribed neoadjuvant imatinib and had a pathogenic complete response. A 41-year-old female patient with … (full text at CIViC)

PMID 37305871 · Rekaya et al., 2023 · Open in CIViC

In this phase II study, 31 patients with histologically confirmed, metastatic GIST who failed after previous treatments involving both imatinib and sunitinib were enrolled. Tumour samples from 20 of t… (full text at CIViC)

PMID 22270258 · Park et al., 2012 · Open in CIViC

This prospective study of 127 patients with metastatic gastrointestinal stromal tumors (GISTs) examined the relationship between kinase (KIT and PDGFRA) genotype and treatment outcome for patients enr… (full text at CIViC)

PMID 14645423 · Heinrich et al., 2003 · Open in CIViC

GIST patients with exon 14 KIT mutations had reduced overall survival compared to patients wiltype for KIT.

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

In a phase III clinical trial comparing different doses of imatinib in GIST patients, KIT exon 9 mutations were associated with significantly improved progression free survival (P=0.0013) and a 61% re… (full text at CIViC)

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

This prospective study of 127 patients with metastatic gastrointestinal stromal tumors (GISTs) examined the relationship between KIT genotype and treatment outcome for patients enrolled in a randomize… (full text at CIViC)

PMID 14645423 · Heinrich et al., 2003 · Open in CIViC

In a prospective phase III study (SWOG S0033/CALGB 150105) of 407 patients with gastrointestinal stromal tumors (GISTs), 397 patients were observed to be CD117-positive (i.e. KIT-positive) and 10 pati… (full text at CIViC)

PMID 18955451 · Heinrich et al., 2008 · 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

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

This patient was from 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 III s… (full text at CIViC)

PMID 18955451 · 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

Patient 3 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 K550_K558 del… (full text at CIViC)

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

Patient 78 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 K550_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

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT K550_W557del primary activating mutation demonstrated sensitivity to imatinib (IC50: 13nmol/L), sunitinib (IC50: 5nmol/L), regor… (full text at CIViC)

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

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT K558NP primary activating mutation demonstrated sensitivity to imatinib (IC50: 2nmol/L), sunitinib (IC50: 2nmol/L ), regorafenib… (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

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

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 47 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 K558_V559 de… (full text at CIViC)

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

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

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