|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
These results suggest that the B-Raf activation segment mutations other than V599E reported in colorectal tumors do not necessarily contribute to carcinogenesis by increasing kinase and transforming activities.
|
14678966 |
2003 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Recently, an alternative pathway of tumorigenesis has been identified in the colorectum associated with serrated precursor lesions, variable levels of microsatellite instability (MSI-V), and driven in part by activating mutations in the BRAF proto-oncogene (V599E).
|
15765445 |
2005 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
BRAF-V600E is not involved in the colorectal tumorigenesis of HNPCC in patients with functional MLH1 and MSH2 genes.
|
15782118 |
2005 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Targeted reduction of mutant (V599E)B-Raf expression (activity) in melanoma cells before tumor formation inhibited tumorigenesis by reducing the growth potential of melanoma cells.
|
15781657 |
2005 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Distribution of BRAF T1799A(V600E) mutations across various types of benign nevi: implications for melanocytic tumorigenesis.
|
18032947 |
2007 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The hot spot c. 1799 T>A, p.V600E gene mutation is very rarely involved in the tumorigenesis of CRC linked to Hereditary Nonpolyposis Colorectal Cancer (HNPCC).
|
17566669 |
2007 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The B-Raf(V600E) mutant, found in 65% of human melanomas, drives constitutive activation of the extracellular signal-regulated kinase (ERK) pathway and is implicated in tumorigenesis.
|
18071315 |
2008 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
In particular, evidence for oncogene-induced melanocyte senescence as natural means to prevent tumorigenesis has been obtained in nevi with mutated B-Raf(V600E).
|
18806824 |
2008 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Our findings provide a molecular linkage between the LKB1-AMPK and the RAF-MEK-ERK pathways and suggest that suppression of LKB1 function by B-RAF V600E plays an important role in B-RAF V600E-driven tumorigenesis.
|
19187764 |
2009 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
These data suggest that the BRAF V600E mutation is not the target gene for abnormal MMR in carcinogenesis in patients with sporadic endometrial cancer, unlike in colon cancer.
|
19424571 |
2009 |
|
Carcinogenesis
|
|
0.100 |
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 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The tumorigenic role of BRAF(V600E) in the development of PTC was documented in thyroid-targeted BRAF(V600E) transgenic mice, and rat thyroid cells overexpressed with BRAF(V600E) suggested that BRAF(V600E) is an initiator of tumorigenesis and is required for tumor progression in PTC.
|
20230995 |
2010 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
To determine the occurrence of BRAF V600E gene mutations and copy number changes of all autosome arms and genes known to be frequently altered in tumorigenesis in primary and metastatic conjunctival melanomas (CoMs).
|
21693616 |
2011 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
In contrast to other Braf-induced mouse models of tumorigenesis (i.e., melanomas and lung), in which knock-in of Braf(V600E) induces mostly benign lesions, Braf-expressing thyrocytes become transformed and progress to invasive carcinomas with a very short latency, a process that is dampened by treatment with an allosteric MEK inhibitor.
|
21220306 |
2011 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Thus, this study uncovered a prominent epigenetic mechanism through which BRAF V600E can promote PTC tumorigenesis by altering the methylation and hence the expression of numerous important genes.
|
21937738 |
2011 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The paradoxically higher incidence of BRAF(V600E) mutations in medium-sized compared with giant CMNs suggests that the presence of the BRAF(V600E) mutation may play different roles between medium and giant CMNs in melanocytic tumorigenesis.
|
21430505 |
2011 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Aberrant signaling of the Ras-Raf-MEK-ERK (MAP kinase) pathway driven by the mutant kinase BRAF(V600E), as a result of the BRAF(T1799A) mutation, plays a fundamental role in thyroid tumorigenesis.
|
21185263 |
2011 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here we report that BRAF(V600E) expression in neural progenitors (NPs) is insufficient for tumorigenesis and increases NP cellular differentiation as well as apoptosis.
|
22586120 |
2012 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The high frequency of methylation and BRAF V600E mutation suggests that many signet ring cell carcinomas may be related to the serrated pathway of carcinogenesis.
|
22522845 |
2012 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The presence of BRAF V600E and mitogen-activated protein kinase activation in a largely benign tumor supports the necessity for secondary events (e.g., p16 loss) in BRAF-driven oncogenesis.
|
22727996 |
2012 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
We combined (L597V)Braf with (G12D)Kras and found that (L597V)Braf modified (G12D)Kras oncogenesis such that fibroblast transformation and lung tumor development were more reminiscent of that driven by the high-activity (V600E)Braf mutant.
|
22892241 |
2012 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
We have thus uncovered a previously unrecognized prominent epigenetic mechanism in the tumorigenesis of melanoma driven by BRAF(V600E).
|
22189819 |
2012 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, we report that Mps1/AKT and B-Raf(WT)/ERK signaling form an auto-regulatory negative feedback loop in melanoma cells; notably, oncogenic B-Raf(V600E) abrogates the negative feedback loop, contributing the aberrant Mps1 functions and tumorigenesis.
|
23726842 |
2013 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
This is the first report of BRAF V600E mutation in endometrial cancer, indicating that it may contribute to tumorigenesis of endometrial cancer, although at a low frequency compared with KRAS mutations.
|
23370429 |
2013 |
|
Carcinogenesis
|
|
0.100 |
GeneticVariation
|
BEFREE |
The prevalence (90%) of the BRAF (V600E) mutation in this study is the highest ever reported, confirming the key role of this mutation in PTC tumorigenesis.
|
23179992 |
2013 |