Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Pharmacological targeting of KIT in gastrointestinal stromal tumours has dramatically changed the clinical outcome of this disease.
|
30792534 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
We hypothesize that based on the allele frequency of SDHA and KIT mutations the tumor is best regarded as SDH-deficient GIST in which the SDHA mutation represents the most likely driver mutation.
|
31124195 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
The tyrosine kinase inhibitor (TKI) imatinib has radically changed the natural history of KIT-driven gastrointestinal stromal tumours (GISTs).
|
31205499 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
AlteredExpression
|
group |
BEFREE |
SIGNIFICANCE: Expression and activity of mutant KIT is essential for driving the majority of GIST neoplasms, which can be therapeutically targeted using BET bromodomain inhibitors.
|
30630822 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
Gastrointestinal stromal tumors (GISTs), a type of mesenchymal tumor in the gastrointestinal tract, are believed to be closely associated with PDGFRA and C-KIT mutations.
|
31647020 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
Resistance to imatinib emerging in patients with GISTs after long-term imatinib treatment does not involve polyclonal expansion of KIT secondary mutations.
|
30126859 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
KIT tyrosine kinase inhibitor, imatinib mesylate, has been successfully used for the treatment of primary, advanced, and disseminated GISTs.
|
28777148 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
Compound 24 displays good antiproliferative effects against c-KIT T670I mutant-driven GIST cell lines (GIST-T1/T670I and GIST-5R) and also exhibits suitable in vivo pharmacokinetic profiles as well as dose-dependent antitumor efficacy.
|
31046271 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Coding exons of KIT and PDGFRA in GISTs with additional malignancies were sequenced.
|
30877378 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
The nodule was resected in an enucleation procedure; subsequent histopathologic examination revealed a low-grade, spindled cell neoplasm with diffuse immunoreactivity for CD117 (cKit) and DOG1, diagnostic of GIST.
|
31497448 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
The results show that efficacy of SU is closely associated with KIT genotypes in GISTs.
|
31083182 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Imatinib, a potent inhibitor of mutated KIT, has revolutionized the clinical management of advanced, metastatic GIST.
|
30523507 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
Mutually exclusive KIT and PDGFRA mutations are considered to be the earliest events in gastrointestinal stromal tumors (GIST), but insufficient for their malignant progression.
|
31553483 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
AlteredExpression
|
group |
BEFREE |
As most GISTs express KIT protein, immunostaining for KIT and/or molecular genetic testing for mutations in KIT can diagnose 95% of GISTs.
|
31577561 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
The tumor was composed of two distinct phenotypes, a CD117 negative region with rhabdomyosarcomatous differentiation directly adjacent to a CD117 positive classic GIST region.
|
31514735 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
AlteredExpression
|
group |
BEFREE |
We also identified a second recurrent insulator loss event near the KIT oncogene, which is also highly expressed across SDH-deficient GISTs.
|
31666694 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
A familial germline mutation in KIT associated with achalasia, mastocytosis and gastrointestinal stromal tumors shows response to kinase inhibitors.
|
31109590 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Currently, the main strategy to combat imatinib resistance is to switch to another tyrosine kinase inhibitor, because imatinib-resistant GIST is usually still oncogenically addicted to KIT/PDGFRA signaling.
|
31308690 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
On the other hand, KIT mutants including KIT<sup>D814Y</sup> in GIST accumulate on the Golgi, and from there, activate downstream.
|
31484543 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
KIT tyrosine kinase inhibitors provide targeted therapy for the underlying genetic mutation, and adjuvant therapy is indicated for patients who are at significant risk of relapse following GIST resection.
|
31550719 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
AlteredExpression
|
group |
BEFREE |
Luciferase assay data in GIST cells, generated using a construct containing all the three miR-221/222 binding sites, are consistent with KIT mRNA levels in GIST patients.
|
30983504 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Genotyping (KIT and PDGFRA) of all but very low-risk GISTs is recommended.
|
31387778 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
This single-arm, multicenter, multinational phase I/II clinical trial (NCT01396148) enrolled eligible patients aged 6 to < 18 years with advanced, unresectable GIST with non-mutant KIT, or who demonstrated disease progression or intolerance to imatinib.
|
31006038 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
GeneticVariation
|
group |
BEFREE |
HQP1351, an orally bioavailable multikinase BCR-ABL inhibitor, is currently in clinical trials for the treatment of T315I mutant chronic myelogenous leukemia (CML), but the potential application in imatinib-resistant GISTs carrying secondary KIT mutations has not been explored.
|
31673329 |
2019 |
Gastrointestinal Stromal Tumors
|
1.000 |
Biomarker
|
group |
BEFREE |
Cyclin D1 inhibition in KIT-independent GISTs had anti-proliferative and pro-apoptotic effects, associated with Rb activation and p27 upregulation.
|
31371779 |
2019 |