Malignant tumor of colon
|
|
0.010 |
GeneticVariation
|
BEFREE |
Relationships between adenomatous polyposis coli (APC) mutations, BRAF V600E mutations, and the CpG island methylator phenotype (CIMP) in colon cancer have not been explored.
|
17293392 |
2007 |
Adenomatous Polyposis Coli
|
|
0.010 |
GeneticVariation
|
BEFREE |
Relationships between adenomatous polyposis coli (APC) mutations, BRAF V600E mutations, and the CpG island methylator phenotype (CIMP) in colon cancer have not been explored.
|
17293392 |
2007 |
Colon Carcinoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Relationships between adenomatous polyposis coli (APC) mutations, BRAF V600E mutations, and the CpG island methylator phenotype (CIMP) in colon cancer have not been explored.
|
17293392 |
2007 |
melanoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
The findings reported here have potential implications for the use of phenothiazines in the treatment of V600E BRAF mutant melanoma.
|
18524847 |
2008 |
Neoplasms
|
|
0.050 |
GeneticVariation
|
BEFREE |
The V600E BRAF mutation was found in 7% of cases and was strongly associated with the tumour features of proximal site, advanced stage and poor histological grade.
|
18778891 |
2009 |
Colorectal Carcinoma
|
|
0.040 |
GeneticVariation
|
BEFREE |
Distinct BRAF (V600E) and KRAS mutations in high microsatellite instability sporadic colorectal cancer in African Americans.
|
19190129 |
2009 |
Malignant neoplasm of colon and/or rectum
|
|
0.020 |
GeneticVariation
|
BEFREE |
Distinct BRAF (V600E) and KRAS mutations in high microsatellite instability sporadic colorectal cancer in African Americans.
|
19190129 |
2009 |
Carcinogenesis
|
|
0.020 |
GeneticVariation
|
BEFREE |
The increased incidence of cancer in FDRs of index CRC patients with the p.V600E BRAF mutation may be explained by a genetic predisposition to develop cancer through the serrated pathway of colorectal carcinogenesis.
|
20570909 |
2010 |
Primary malignant neoplasm
|
|
0.010 |
GeneticVariation
|
BEFREE |
The increased incidence of cancer in FDRs of index CRC patients with the p.V600E BRAF mutation may be explained by a genetic predisposition to develop cancer through the serrated pathway of colorectal carcinogenesis.
|
20570909 |
2010 |
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
The increased incidence of cancer in FDRs of index CRC patients with the p.V600E BRAF mutation may be explained by a genetic predisposition to develop cancer through the serrated pathway of colorectal carcinogenesis.
|
20570909 |
2010 |
Colorectal Carcinoma
|
|
0.040 |
GeneticVariation
|
BEFREE |
Activating V600E mutation in BRAF gene has been linked with widespread methylation of CpG islands in sporadic colorectal cancers.
|
21455633 |
2011 |
Neoplasms
|
|
0.050 |
GeneticVariation
|
BEFREE |
We propose that continuously activated BRAF(V600E) signaling may be a possible mechanism for the deregulation of Mps1 stability and kinase activity in human tumors, and that persistent phosphorylation of Mps1 through BRAF(V600E) signaling is a key event in disrupting the control of centrosome duplication and chromosome stability that may contribute to tumorigenesis.
|
22430208 |
2013 |
Carcinogenesis
|
|
0.020 |
GeneticVariation
|
BEFREE |
We propose that continuously activated BRAF(V600E) signaling may be a possible mechanism for the deregulation of Mps1 stability and kinase activity in human tumors, and that persistent phosphorylation of Mps1 through BRAF(V600E) signaling is a key event in disrupting the control of centrosome duplication and chromosome stability that may contribute to tumorigenesis.
|
22430208 |
2013 |
polyps
|
|
0.010 |
GeneticVariation
|
BEFREE |
BRAF((V600E)) mutation is not a frequent event in right colon serrated polyps in a subset of the Chinese population.
|
24570042 |
2014 |
Neoplasms
|
|
0.050 |
GeneticVariation
|
BEFREE |
Further, we analyzed the protein expression of V600E mutated BRAF, MLH1, MSH2, MSH6 and p53 from a larger set of PMP tumors (n = 74) using immunohistochemistry.
|
25274248 |
2015 |
Neoplasms
|
|
0.050 |
GeneticVariation
|
BEFREE |
Commonly observed alterations across sporadic CRCs have allowed classification into a (1) hypermutated group that includes defective DNA mismatch repair with microsatellite instability and POLE mutations in ∼15%, containing multiple frameshifted genes and BRAF(V600E); (2) nonhypermutated group with multiple somatic copy number alterations and aneuploidy in ∼85%, containing oncogenic activation of KRAS and PIK3CA and mutation and loss of heterozygosity of tumor suppressor genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in ∼20% that overlap greatly with microsatellite instability CRCs and some nonhypermutated CRCs; and (4) elevated microsatellite alterations at selected tetranucleotide repeats in ∼60% that associates with metastatic behavior in both hypermutated and nonhypermutated groups.
|
26216840 |
2015 |
Colorectal Carcinoma
|
|
0.040 |
GeneticVariation
|
BEFREE |
Commonly observed alterations across sporadic CRCs have allowed classification into a (1) hypermutated group that includes defective DNA mismatch repair with microsatellite instability and POLE mutations in ∼15%, containing multiple frameshifted genes and BRAF(V600E); (2) nonhypermutated group with multiple somatic copy number alterations and aneuploidy in ∼85%, containing oncogenic activation of KRAS and PIK3CA and mutation and loss of heterozygosity of tumor suppressor genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in ∼20% that overlap greatly with microsatellite instability CRCs and some nonhypermutated CRCs; and (4) elevated microsatellite alterations at selected tetranucleotide repeats in ∼60% that associates with metastatic behavior in both hypermutated and nonhypermutated groups.
|
26216840 |
2015 |
Pseudomyxoma Peritonei
|
|
0.010 |
GeneticVariation
|
BEFREE |
Further, we analyzed the protein expression of V600E mutated BRAF, MLH1, MSH2, MSH6 and p53 from a larger set of PMP tumors (n = 74) using immunohistochemistry.
|
25274248 |
2015 |
Hereditary Nonpolyposis Colorectal Cancer
|
|
0.010 |
GeneticVariation
|
BEFREE |
We defined sporadic MSI-high carcinomas as those with loss of MLH1 and PMS2 immunostaining and BRAF V600E mutations that occurred in patients 50 years of age or older without a family history of colonic adenocarcinoma or Lynch syndrome.
|
25602793 |
2015 |
Rhabdoid meningioma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Metastatic rhabdoid meningioma with BRAF V600E mutation and good response to personalized therapy: case report and review of the literature.
|
25116269 |
2015 |
MSI-high
|
|
0.010 |
GeneticVariation
|
BEFREE |
We defined sporadic MSI-high carcinomas as those with loss of MLH1 and PMS2 immunostaining and BRAF V600E mutations that occurred in patients 50 years of age or older without a family history of colonic adenocarcinoma or Lynch syndrome.
|
25602793 |
2015 |
Papillary Meningioma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Metastatic rhabdoid meningioma with BRAF V600E mutation and good response to personalized therapy: case report and review of the literature.
|
25116269 |
2015 |
Lynch Syndrome
|
|
0.010 |
GeneticVariation
|
BEFREE |
We defined sporadic MSI-high carcinomas as those with loss of MLH1 and PMS2 immunostaining and BRAF V600E mutations that occurred in patients 50 years of age or older without a family history of colonic adenocarcinoma or Lynch syndrome.
|
25602793 |
2015 |
Gastro-enteropancreatic neuroendocrine tumor
|
|
0.010 |
GeneticVariation
|
BEFREE |
In conclusion, BRAF V600E mutation is likely to result in resistance to pazopanib but may be a potentianally actionable mutation in metastatic GEP-NETs patients.
|
26684240 |
2016 |
Malignant transformation
|
|
0.010 |
GeneticVariation
|
BEFREE |
Our results also provide evidence that--just as BRAF V600E mutations in hyperplastic polyps and benign nevi- a mutated driver gene does not imply malignant behavior per se but may set the basis for malignant transformation.
|
26493284 |
2016 |