Soft Tissue Neoplasm

KIT encodes a receptor tyrosine kinase comprised of an extracellular domain, a transmembrane domain, and a cytoplasmic tyrosine kinase domain. Upon binding of its ligand, mast cell growth factor (MGF,… (full text at CIViC)

PMID 20533592 · Bayraktar et al., 2010 · Open in CIViC

When transiently transfected into Chinese hamster ovary cells, the KIT exon 9 mutants were ten times less sensitive to imatinib in comparison to the KIT exon 11 mutants as measured by autophosphorylat… (full text at CIViC)

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

In a prospective study of 137 gastrointestinal stromal tumor patients who failed imatinib treatment, patients with KIT exon 9 mutations (15/89) treated with sunitinib were associated with improved pr… (full text at CIViC)

PMID 22439647 · Rutkowski et al., 2012 · Open in CIViC

In a retrospective study, Chinese gastrointestinal stromal tumor patients harboring KIT S501_A502insAY in-frame insertion mutation (n=2) were associated with improved response to sunitinib treatment a… (full text at CIViC)

PMID 23456621 · Gao et al., 2013 · Open in CIViC

In a retrospective study of 3 gastrointestinal stromal tumor patients harboring KIT S501_A502insAY in-frame insertion mutation, KIT S501_A502insAY was associated with improved response to sunitinib tr… (full text at CIViC)

PMID 19861442 · Guo et al., 2009 · Open in CIViC

In a retrospective study of 23 Taiwanese gastrointestinal stromal tumor patients who failed imatinib therapy or were imatinib intolerant, patients with KIT exon 9 mutation ((n=6/21) were associated wi… (full text at CIViC)

PMID 21547131 · Chen et al., 2011 · Open in CIViC

In an in vitro study, a 32D cell line expressing KIT S501_A502insAY mutation (overexpression) demonstrated increased sensitivity to sunitinib treatment (IC50: 10.9nM) similar to 32D cells expressing w… (full text at CIViC)

PMID 24205792 · Zhao et al., 2014 · 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

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

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 123 metastatic or advanced gastrointestinal stromal tumor patients with KIT exon 11 mutations, patients with KIT exon 11 mutations were reported to be responsive to sunitin… (full text at CIViC)

PMID 26416414 · Vincenzi 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

In an in vitro study, an IL3 independent Ba/F3 cell line expressing KIT V560D primary activating mutation demonstrated sensitivity to imatinib (IC50: 3nmol/L), sunitinib (IC50: 2nmol/L), regorafenib (… (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

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