Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE The proliferation and tumorigenesis in V600E melanoma were decrease after CPT1A knockdown. 27793752

2016

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE The coexistence of LCH and ECD in the same biopsy and the BRAF (V600E) mutation status in both histologic types support the recent re-classification of the histiocytic disorder into LCH, ECD, and "mixed histiocytosis", which reflects tumorigenesis for all three from a common progenitor cell. 26466952

2016

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 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

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE Therefore, these data indicate that PRDX1 and PRDX6 expression not only may play a key role in papillary thyroid carcinogenesis via a BRAF V600E-dependent mechanism, but their determination could be considered as potential tumor marker for indicating tumor progression in PTCs, independently of BRAF status. 24316730

2014

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE BRAF(V600E) mutation is an early event in thyroid carcinogenesis, and is associated with distinctive morphology and aggressive features even in papillary thyroid microcarcinomas. 22918165

2013

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE To understand how oncogenic B-Raf contributes to carcinogenesis, in particular to aspects other than cellular proliferation and survival, we generated three isogenic human colorectal carcinoma cell line models in which we can dynamically modulate the expression of the B-Raf(V600E) oncoprotein. 25381152

2015

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
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

dbSNP: rs121913377
rs121913377
0.100 GeneticVariation BEFREE Further analyses suggested a complex mechanism driven by mutation BRAF (V600E) on melanoma tumorigenesis that disturbs specific cancer-related genes, pathways, and methylation modifications. 25890285

2015