Stromal Neoplasm

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

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