|
rs11554290
|
|
melanoma
|
C |
0.800 |
CausalMutation
|
CLINVAR |
NRAS-mutant melanoma: response to chemotherapy.
|
21576590 |
2011 |
|
rs11554290
|
|
melanoma
|
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 |
|
rs11554290
|
|
melanoma
|
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 |
|
rs11554290
|
|
melanoma
|
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 |
|
rs11554290
|
|
melanoma
|
C |
0.800 |
CausalMutation
|
CLINVAR |
MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study.
|
23414587 |
2013 |
|
rs11554290
|
|
melanoma
|
A |
0.800 |
CausalMutation
|
CLINVAR |
MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study.
|
23414587 |
2013 |
|
rs11554290
|
|
melanoma
|
G |
0.800 |
CausalMutation
|
CLINVAR |
MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: a non-randomised, open-label phase 2 study.
|
23414587 |
2013 |
|
rs11554290
|
|
melanoma
|
G |
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 |
|
rs11554290
|
|
melanoma
|
A |
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 |
|
rs11554290
|
|
melanoma
|
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 |
|
rs11554290
|
|
melanoma
|
C |
0.800 |
CausalMutation
|
CLINVAR |
Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.
|
23569304 |
2013 |
|
rs11554290
|
|
melanoma
|
A |
0.800 |
CausalMutation
|
CLINVAR |
Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.
|
23569304 |
2013 |
|
rs11554290
|
|
melanoma
|
G |
0.800 |
CausalMutation
|
CLINVAR |
Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.
|
23569304 |
2013 |
|
rs11554290
|
|
melanoma
|
G |
0.800 |
CausalMutation
|
CLINVAR |
Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors.
|
23614898 |
2013 |
|
rs11554290
|
|
melanoma
|
C |
0.800 |
CausalMutation
|
CLINVAR |
Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors.
|
23614898 |
2013 |
|
rs11554290
|
|
melanoma
|
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 |
|
rs11554290
|
|
melanoma
|
|
0.800 |
GeneticVariation
|
BEFREE |
Besides confirming the presence of known melanoma driver mutations (BRAF(V600E), NRAS(Q61R) ), we identified novel mutated genes involved in signalling pathways crucial for melanoma pathogenesis and already addressed by current targeted therapies (such as MAPK and glutamate pathways).
|
23704925 |
2013 |
|
rs11554290
|
|
melanoma
|
|
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 |
|
rs11554290
|
|
melanoma
|
|
0.800 |
GeneticVariation
|
BEFREE |
We investigated the associations between BRAF(V600E) and NRAS(Q61R) mutations and known risk factors, clinicopathologic characteristics and clinical outcomes of melanoma in a case series of primary invasive cutaneous melanoma from the Nurses' Health Study (NHS).
|
25048604 |
2014 |
|
rs11554290
|
|
melanoma
|
C |
0.800 |
CausalMutation
|
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
rs11554290
|
|
melanoma
|
A |
0.800 |
CausalMutation
|
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
rs11554290
|
|
melanoma
|
G |
0.800 |
CausalMutation
|
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
rs11554290
|
|
melanoma
|
|
0.800 |
GeneticVariation
|
BEFREE |
Formalin-fixed and paraffin-embedded melanoma tissues were analyzed for BRAF and NRAS mutations by independent, blinded observers using both conventional DNA molecular techniques and immunohistochemistry with the novel anti-human N-Ras (Q61R) monoclonal antibody (clone SP174).
|
25341653 |
2015 |
|
rs11554290
|
|
melanoma
|
|
0.800 |
GeneticVariation
|
BEFREE |
Here, we report that guanosine monophosphate synthase (GMPS), an enzyme required for the de novo biosynthesis of GMP, has a major role in invasion and tumorigenicity of cells derived from either BRAF(V600E) or NRAS(Q61R) human metastatic melanomas.
|
25909885 |
2015 |
|
rs11554290
|
|
melanoma
|
|
0.800 |
GeneticVariation
|
BEFREE |
In our study, we showed that combining immunohistochemistry analysis targeting NRAS(Q61R) and BRAF(V600E) proteins with molecular analysis was a reliable theranostic tool to face challenging samples of melanoma.
|
26204954 |
2015 |