|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The results of this study suggested that Apa/p NPs could inhibit the growth of melanoma tumors by inhibiting the phosphorylation and expression of VEGFR-2 and downstream ERK1/2, providing a theoretical basis for the clinical application of Apatinib in the treatment of melanoma.
|
31668370 |
2020 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
SIGNIFICANCE: Activation of the IGF1R-MEK5-Erk5 signaling pathway opposes pharmacologic inhibition of Erk1/2 in melanoma, leading to the reactivation of cell proliferation and acquired resistance.
|
30833419 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dehydrocorydaline inhibits cell proliferation, migration and invasion via suppressing MEK1/2-ERK1/2 cascade in melanoma.
|
31456643 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
ERK1 is the immediate downstream target of MEK1/2, which is druggable with trametinib, an approved therapeutic for melanoma.
|
30804427 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Plk1 inhibition induced apoptosis in CRTs, leading to slowed growth of BRAF and MEK inhibitor-resistant tumors <i>in vivo</i> These data demonstrate the utility of <i>in vivo</i> ERK1/2 pathway reporting as a tool to optimize clinical dosing schemes and establish suppression of Plk1 as potential salvage therapy for BRAF inhibitor and MEK inhibitor-resistant melanoma.
|
31270153 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study aimed to explore the relationship of HO-1 and B-Raf via mediating ERK1/2 signaling on cell cycle in melanoma.
|
30634993 |
2019 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
High affinity inhibitors of ERK1/2 have been shown in preclinical studies to bypass the resistance of melanoma and colon cancer cells to BRAF and MKK1/2 inhibitors, and are thus promising additions to current treatment protocols.
|
29255136 |
2018 |
|
melanoma
|
0.100 |
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of p38 and ERK1/2 pathways by Sparstolonin B suppresses inflammation-induced melanoma metastasis.
|
29276966 |
2018 |
|
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our study indicates that targeting the nuclear translocation of ERK1/2, in combination with MEK inhibitors can be used for the treatment of different mutant melanomas.
|
29180761 |
2017 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, our data demonstrate the pro-tumorigenic role of KLF4 in melanoma and uncover a novel ERK1/2-E2F1-KLF4 axis.
|
28068326 |
2017 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
NRAS(wild-type) /BRAF(wild-type) melanoma metastases are characterized by significant gains of MAP2K1 (MEK1) and MAPK3 (ERK1) gene loci.
|
26684394 |
2016 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The ERK1/2-MAPK pathway is critical for cutaneous melanoma development and consequently an important therapeutic target.
|
27166257 |
2016 |
|
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Several transcription factors and signaling pathways involved in the regulation of MITF expression and/or activity such as the Wnt/β-catenin pathway are broadly utilized by various types of tumors, whereas others, e.g., BRAF(V600E)/ERK1/2 are more specific for melanoma.
|
25433395 |
2015 |
|
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We sought to preemptively determine mutations in ERK1/2 that confer resistance to either ERK inhibitors or combined RAF/MEK inhibition in BRAF(V600)-mutant melanoma.
|
25320010 |
2014 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mutations in the v-raf murine sarcoma viral oncogene homolog B1 (BRAF) gene occur frequently in melanoma and lead to constitutive activation of the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK1/2) pathway.
|
25026375 |
2014 |
|
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, recently identified ERK1/2-inducing mutations in MEK1 and MEK2 (MEK1/2) MAPK genes in melanoma confer resistance to emerging therapeutic MEK inhibitors, underscoring the challenges facing direct kinase inhibition in cancer.
|
23603816 |
2013 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Activation of the ERK1/2 mitogen-activated protein kinases (MAPK) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas.
|
24121492 |
2013 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Somatic GNAQ mutations at codon 209 have been identified in approximately 50% of uveal melanomas and have been reported to be oncogenic through activating PLCβ/PKC/Erk1/2 pathways.
|
22653968 |
2012 |
|
melanoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
When assessing the functionality of the EpoR-signaling pathway, recombinant human Epo led to the phosphorylation of JAK-2, signal transducers and activators of transcription 3 (STAT3), and ERK1/2 in several of the melanoma cell lines that were analyzed.
|
19536148 |
2010 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MCSP expression in melanoma cells enhances integrin function and constitutive activation of Erk1,2.
|
19738072 |
2009 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Thus MEK-PKCalpha-ERK1/2 and PI3-K/Akt survival pathways are activated in EC cultures during the interaction with CM from both melanoma cell lines, providing new insight in understanding EC metabolism and signaling.
|
19747926 |
2009 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CXCR1- or CXCR2-induced modulation of melanoma cell proliferation and migration was observed to be mediated through the activation of ERK1/2 phosphorylation.
|
19401689 |
2009 |
|
melanoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Melanoma cell lines expressing (WT)B-Raf and (WT)Ras grew with similar proliferation rates, showed constitutive activation of ERK1/2, and had similar levels of B-Raf expression and B-Raf kinase activity as melanoma cell lines expressing the activating V600E mutation ((V600E)B-Raf).
|
16452469 |
2006 |
|
melanoma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
In conclusion, our results indicate that the protective effect of PMA on anchorage-independent survival of melanoma cells at least partly is mediated by MEK-independent activation of ERK1/2 and inactivation of downstream pro-apoptotic effector proteins.
|
15721302 |
2005 |