Soft Tissue Neoplasm

In an in vitro study, a 32D cell line expressing KIT D579_H580insIDPTQLPYD mutation (overexpression) demonstrated reduced sensitivity to sunitinib treatment (IC50: 47.4nM) compared to 32D cells expres… (full text at CIViC)

PMID 24205792 · Zhao et al., 2014 · Open in CIViC

Several preclinical studies were done in order to test the effects of various tyrosine kinase inhibitors (TKIs) on KIT-mutant cell lines derived from Gastrointestinal Stromal Tumor (GIST) patients wit… (full text at CIViC)

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

A preclinical study was done in order to test the effects of a tyrosine kinase inhibitor (TKI) on the ponatinib-sensitive KIT-mutant cell line GIST-T1 derived from Gastrointestinal Stromal Tumor (GIST… (full text at CIViC)

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

Ponatinib possesses potent activity against D816G KIT mutant in preclinical experiments.

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

In an in vitro study, a Ba/F3 cell line expressing KIT W557_K558del primary mutation (known to confer sensitivity to regorafenib) and KIT D816G secondary mutation, KIT D816G was associated with decrea… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · 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 D816H KIT mutant in preclinical experiments.

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

In an in vitro study, a 32D cell line expressing KIT D816V mutation (overexpression) demonstrated reduced sensitivity to sunitinib treatment (IC50: 294.7nM) compared to 32D cells expressing wild-type … (full text at CIViC)

PMID 24205792 · Zhao et al., 2014 · Open in CIViC

Sunitinib has shown efficacy against certain imatinib-resistant mutants, although a subset that resides in the activation loop, including D816H/V, remains resistant. Biochemical and structural studies… (full text at CIViC)

PMID 19164557 · Gajiwala et al., 2009 · Open in CIViC

In an in vitro study, a Ba/F3 cell line expressing KIT 557-558del primary mutation (known to confer sensitivity to regorafenib) was incubated in various concentrations of ponatinib, sunitinib, or rego… (full text at CIViC)

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

In an in vitro study, a 32D cell line expressing KIT D816Y mutation (overexpression) demonstrated reduced sensitivity to sunitinib treatment (IC50: 73.1nM) compared to 32D cells expressing wild-type K… (full text at CIViC)

PMID 24205792 · Zhao et al., 2014 · 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

In an in vitro study, Ba/F3 cell lines expressing KIT primary mutations and KIT D820A secondary mutation, KIT D820A was associated with similar sensitivity to ponatinib treatment compared to Ba/F3 cel… (full text at CIViC)

PMID 25239608 · Garner et al., 2014 · 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

This retrospective study of a phase 2 clinical trial (NCT01068769) examined regorafenib safety and efficacy in advanced gastrointestinal stromal tumor (GIST) patients refractory to at least imatinib a… (full text at CIViC)

PMID 22614970 · George 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

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

Patients with Exon 11 Kit mutations (N=85) had significantly better event-free and overall survival than patients with Exon 9 Kit mutations (N=23) or no Kit mutations (N=9).

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

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…

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