Source: ALL
Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors. 23614898

2013
dbSNP: rs11554290
rs11554290
NRAS
0.800 GeneticVariation BEFREE Mutation in BRAF and NRAS was present in 43% (88% V600E, 10% V600K) and 30% (48% Q61K, 40% Q61R) of metastatic melanomas, respectively. 23855428

2013
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR Inhibition of Wee1, AKT, and CDK4 underlies the efficacy of the HSP90 inhibitor XL888 in an in vivo model of NRAS-mutant melanoma. 23538902

2013
dbSNP: rs11554290
rs11554290
NRAS
G 0.800 CausalMutation CLINVAR First-in-human, phase I dose-escalation study of the safety, pharmacokinetics, and pharmacodynamics of RO5126766, a first-in-class dual MEK/RAF inhibitor in patients with solid tumors. 22761467

2012
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR First-in-human, phase I dose-escalation study of the safety, pharmacokinetics, and pharmacodynamics of RO5126766, a first-in-class dual MEK/RAF inhibitor in patients with solid tumors. 22761467

2012
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR First-in-human, phase I dose-escalation study of the safety, pharmacokinetics, and pharmacodynamics of RO5126766, a first-in-class dual MEK/RAF inhibitor in patients with solid tumors. 22761467

2012
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR NRAS-mutant melanoma: response to chemotherapy. 21576590

2011
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR NRAS-mutant melanoma: response to chemotherapy. 21576590

2011
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. 20179705

2010
dbSNP: rs11554290
rs11554290
NRAS
0.800 GeneticVariation BEFREE We have evaluated five real-time ARMS assays: BRAF 1799T>A, [this includes V600E and V600K] and NRAS 182A>G [Q61R] and 181C>A [Q61K] in melanoma, EGFR 2573T>G [L858R], 2235-2249del15 [E746-A750del] in non-small-cell lung cancer, and compared the results to DNA sequencing of the mutation 'hot-spots' in these genes in formalin-fixed paraffin-embedded tumour (FF-PET) DNA. 20925915

2010
dbSNP: rs11554290
rs11554290
NRAS
G 0.800 CausalMutation CLINVAR RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth. 20130576

2010
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. 20179705

2010
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth. 20130576

2010
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. 21107323

2010
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR Furthermore, PLX4032 increased the rate of proliferation of growth factor-dependent NRAS Q61L mutant primary melanoma cells, reduced cell adherence and increased mobility of cells from advanced lesions. 20149136

2010
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032. 20406486

2010
dbSNP: rs11554290
rs11554290
NRAS
G 0.800 CausalMutation CLINVAR RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. 20179705

2010
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth. 20130576

2010
dbSNP: rs11554290
rs11554290
NRAS
0.800 GeneticVariation BEFREE Reciprocally, overexpression of C-MYC in normal melanocytes suppressed BRAF(V600E)-induced senescence more efficiently than NRAS(Q61R)-induced senescence, which agrees with the generally higher rates of activating mutations in BRAF than NRAS gene in human cutaneous me</span>lanomas. 18679422

2008
dbSNP: rs11554290
rs11554290
NRAS
A 0.800 CausalMutation CLINVAR Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers. 18390968

2008
dbSNP: rs11554290
rs11554290
NRAS
G 0.800 CausalMutation CLINVAR Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers. 18390968

2008
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers. 18390968

2008
dbSNP: rs11554290
rs11554290
NRAS
C 0.800 CausalMutation CLINVAR Distinct sets of genetic alterations in melanoma. 16291983

2005
dbSNP: rs11554290
rs11554290
NRAS
0.800 GeneticVariation BEFREE We studied global gene expression in three melanoma cell lines with the most common and potent V600E mutation in the B-RAF gene-four cell lines with a common Q61R mutation in the N-RAS gene and three cell lines with no mutations using human HG-U133A 2.0 micro-arrays with 22 277 transcripts. 15760917

2005
dbSNP: rs11554290
rs11554290
NRAS
G 0.800 CausalMutation CLINVAR Distinct sets of genetic alterations in melanoma. 16291983

2005