|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Larger studies are required to corroborate whether BRAF mutation may predict sorafenib resistance in GISTs.
|
30179868 |
2019 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
Biomarker
|
group |
BEFREE |
Following the successes of BRAF-targeted therapy in melanoma and KIT-targeted therapy in gastrointestinal stromal tumors, small-molecule tyrosine kinase inhibitors targeting KIT have been examined in KIT-mutated melanoma.
|
30707374 |
2019 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
New mutated genes (<i>CDK4</i>, <i>AKT2</i>, <i>FLT3</i>, <i>ERBB2</i>, <i>ABL1</i> and <i>AKT1</i>), a higher <i>BRAF</i> mutation frequency (7.5%) and new BRAF mutation sites (G464E) were found in Chinese GIST patients.
|
29719410 |
2018 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
The majority of gastrointestinal stromal tumors (GIST) are driven by KIT, PDGFRA, or, less commonly, BRAF mutations, and SDH gene inactivation is involved in a limited fraction of gastric lesions.
|
27390349 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
We conclude that genome analysis of wild-type GISTs for mutations should include the BRAF gene, as its mutation status contributes to understanding of pathogenesis and might be important for decisions on therapy.
|
27864688 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
In our study, we aimed at analyzing a large cohort (n=444) of GISTs for BRAF mutations using molecular and immunohistochemical methods.
|
28159677 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Secondary resistance to IM in GISTs typically occurs due to several mechanisms that include hemi- or homo-zygous deletion of the wild-type KIT allele, overexpression of focal adhesion kinase (FAK) and insulin-like growth factor receptor I (IGF-1R) amplification, BRAF mutation, a RTK switch (loss of c-KIT and gain of c-MET/AXL), etc.
|
29206199 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
This clinicopathologic heterogeneity is paralleled by an underlying molecular diversity: the majority of GISTs are associated with spontaneous activating mutations in KIT, PDGFRA, or BRAF, while additional subsets are driven by genetic lesions-often inherited-of NF1 or components of the succinate dehydrogenase enzymatic complex.
|
28820749 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
GISTs with the BRAF V600E mutation are relatively benign tumors with a distinctive molecular mechanism.
|
28034324 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
Biomarker
|
group |
BEFREE |
Regarding the <i>KIT/PDGFRA</i>/B-Raf proto-oncogene, serine/threonine kinase molecular profile of the 79 GISTs, 83.6% of the tumors possessed <i>KIT</i> mutations, 10.1% had <i>PDGFRA</i> mutations and 6.3% were triple wild-type.
|
29113157 |
2017 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Concomitant KIT/BRAF and PDGFRA/BRAF mutations are rare events in gastrointestinal stromal tumors.
|
27097112 |
2016 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
GIST with BRAF mutation arises in the small intestine.
|
27427238 |
2016 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
BRAF and NF-1 mutated GISTs do not have any characteristic morphological features.
|
27317811 |
2016 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
BRAF V600E mutation-specific immunohistochemistry is a highly sensitive and specific method for detecting BRAF-mutated GISTs.
|
26486743 |
2015 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Our purpose is to define the distribution of c-KIT, PDGFR and BRAF mutations in a population-based cohort of gastrointestinal stromal tumors (GIST) patients and correlate them with anatomical site, risk classification and survival.
|
25885906 |
2015 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
Biomarker
|
group |
BEFREE |
A preliminary study of the BRAF VE1 antibody showed non-specific staining, and indicated it was neither a specific nor a sensitive marker of wild-type GISTs.
|
25659413 |
2015 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Recently, activating BRAF mutation was detected in a small percentage of GISTs.
|
25182956 |
2015 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Mutation was a significant prognostic indicator of overall survival in naive, localized GISTs (P<0.001): KIT-mutated patients had a worse outcome than PDGFRA-mutated or triple-negative (KIT, PDGFRA, BRAF wild-type) cases.
|
25970686 |
2015 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
Biomarker
|
group |
BEFREE |
The molecular biology of these GIST, originally defined as KIT/PDGFRA wild-type (WT), is complex due to the existence of different subgroups with distinct molecular hallmarks, including defects in the succinate dehydrogenase (SDH) complex and mutations of neurofibromatosis type 1 (NF1), BRAF, or KRAS genes (RAS-pathway or RAS-P).In this extremely heterogeneous landscape, the clinical profile and molecular abnormalities of the small subgroup of WT GIST suitably referred to as quadruple wild-type GIST (quadrupleWT or KITWT/PDGFRAWT/SDHWT/RAS-PWT) remains undefined.
|
25239601 |
2014 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
Biomarker
|
group |
BEFREE |
Median time to resistance to targeted agents occurs in ~7 months with BRAF inhibitors and 2 years for imatinib in GIST.
|
24531699 |
2014 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Other uncommon genetic groups include neurofibromatosis type I-associated and BRAF-mutant GISTs.
|
24117705 |
2014 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
We constructed tissue microarrays of formalin-fixed and paraffin-embedded specimens of 534 gastroesophageal tumors (119 squamous cell cancers and 72 adenocarcinomas of the esophagus, 63 cancers of the gastroesophageal junction/cardia, 199 gastric cancers of the corpus or antrum, 81 gastric gastrointestinal stromal tumors) and performed anti-BRAF-V600E immunostaining using the mutation-specific antibody VE1.
|
23343956 |
2013 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
We report prolonged antitumor activity in the first patient with V600E BRAF-mutated GIST who was treated with a BRAF inhibitor.
|
23470635 |
2013 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
CausalMutation
|
group |
CLINVAR |
BRAF mutant gastrointestinal stromal tumor: first report of regression with BRAF inhibitor dabrafenib (GSK2118436) and whole exomic sequencing for analysis of acquired resistance.
|
23470635 |
2013 |
|
Gastrointestinal Stromal Tumors
|
0.500 |
GeneticVariation
|
group |
BEFREE |
No significant differences were found when comparing DOG-1 and c-KIT expression in WT, SDHB-mutated and KIT/PDGFRA/BRAF-mutated GISTs.
|
22948025 |
2013 |