|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
While the role of the BRAF-MEK1/2-ERK1/2 pathway in melanoma is well established, the involvement of mitogen-activated protein kinases MEK5-ERK5 remains poorly explored.
|
29483645 |
2018 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
We thus report for the first time a low prevalence of MEK1 mutations in melanoma and colon cancer.
|
19411838 |
2009 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
We found that the acquired MEK1-C121S mutation in BRAF-V600E mutant melanoma conferred resistance to both vemurafenib and selumetinib but not E6201.
|
24448821 |
2014 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Together, these pathways provide a way to activate MAPK signaling downstream of BRAF and MEK1 inhibitors, which are commonly used to treat melanoma.
|
30543563 |
2019 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
To compare the efficacy and tolerability of the mitogen-activated protein (MAP)/extracellular signal-regulated (ERK) kinase (MEK) 1/2 inhibitor selumetinib versus temozolomide in chemotherapy-naive patients with unresectable stage III/IV melanoma.
|
22048237 |
2012 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Thus, activating MEK1 exon 3 mutations identified herein and concurrent with V600E/KBRAF do not cause BRAFi resistance in melanoma.
|
22588879 |
2012 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
This MEK1(T55delins) (RT) mutation could be traced back to a fraction of the pre-treatment lesion and not only provided protection against vemurafenib but also promoted local invasion of transplanted melanomas.
|
26105199 |
2015 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
The purpose of this study was to determine the response rate (RR) for the selective, allosteric MEK1/MEK2 inhibitor trametinib (GSK1120212), in patients with metastatic BRAF-mutant melanoma.
|
23248257 |
2013 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
The mitogen-activated extracellular signal-regulated kinase 1/2 (MEK1/2) inhibitor trametinib has shown promising therapeutic effects on melanoma, but its efficacy on colorectal cancer (CRC) is limited.
|
28756770 |
2017 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Targeting BMK1 Impairs the Drug Resistance to Combined Inhibition of BRAF and MEK1/2 in Melanoma.
|
28387310 |
2017 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Taken together, our data indicate that preexisting MEK1(P124) mutations are associated with a reduced response to BRAF inhibitor therapy and identify a subset of patients with BRAF-mutant melanoma likely to benefit from combination therapies involving MEK or ERK inhibitors.
|
25370473 |
2015 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
LHGDN |
Surprisingly, MEK1 and ERK1/2 activities were restored in integrin alphav-negative melanoma cells by suppression of p53, whereas concomitant block of MEK1 induced apoptosis.
|
15557124 |
2004 |
|
melanoma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
Single treatment of BRAF mutant melanoma cell lines with vemurafenib or dabrafenib (BRAF inhibitors) alone or in combination with trametinib (MEK1/2 inhibitor) resulted in overexpression of Mcl-1.
|
26497853 |
2015 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Screening a larger cohort of individuals with melanoma revealed the presence of recurring somatic MAP2K1 and MAP2K2 mutations, which occurred at an overall frequency of 8%.
|
22197931 |
2011 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
CTD_human |
Screening a larger cohort of individuals with melanoma revealed the presence of recurring somatic MAP2K1 and MAP2K2 mutations, which occurred at an overall frequency of 8%.
|
22197931 |
2011 |
|
melanoma
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Screening a larger cohort of individuals with melanoma revealed the presence of recurring somatic MAP2K1 and MAP2K2 mutations, which occurred at an overall frequency of 8%.
|
22197931 |
2011 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Recent clinical and therapeutic success with RAF and MEK1/2 inhibitors has revolutionized the existing treatment schemes for previously incurable cancers like melanomas.
|
31662208 |
2019 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
melanoma
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
melanoma
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors.
|
22588879 |
2012 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
PI3'-kinase inhibition forestalls the onset of MEK1/2 inhibitor resistance in BRAF-mutated melanoma.
|
25472943 |
2015 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Phase II trial of MEK inhibitor selumetinib (AZD6244, ARRY-142886) in patients with BRAFV600E/K-mutated melanoma.
|
23444215 |
2013 |
|
melanoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
phase II and III clinical trials demonstrated modest anti- tumor activity of Binimetinib (MEK162) - a potent allosteric inhibitor of MEK1 and MEK2- in patients with advanced NRAS mutant melanoma.
|
28919996 |
2017 |
|
melanoma
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.
|
23569304 |
2013 |
|
melanoma
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Pharmacodynamic effects and mechanisms of resistance to vemurafenib in patients with metastatic melanoma.
|
23569304 |
2013 |