rs113994087
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|
0.100 |
GeneticVariation |
BEFREE |
A 77-gene ALK signature was established and successfully validated in primary neuroblastoma samples, in a neuroblastoma cell line with ALK(F1174L) and ALK(R1275Q) regulable overexpression constructs and in other ALKomas.
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25805801 |
2015 |
rs281864719
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|
|
0.100 |
GeneticVariation |
BEFREE |
A 77-gene ALK signature was established and successfully validated in primary neuroblastoma samples, in a neuroblastoma cell line with ALK(F1174L) and ALK(R1275Q) regulable overexpression constructs and in other ALKomas.
|
25805801 |
2015 |
rs863225281
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|
|
0.100 |
GeneticVariation |
BEFREE |
A 77-gene ALK signature was established and successfully validated in primary neuroblastoma samples, in a neuroblastoma cell line with ALK(F1174L) and ALK(R1275Q) regulable overexpression constructs and in other ALKomas.
|
25805801 |
2015 |
rs281864719
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|
|
0.100 |
GeneticVariation |
BEFREE |
Accordingly, the combination of the ALK/MET inhibitor crizotinib and selective HDAC8 inhibitors (3-6 µM PCI-34051 or 10 µM 20a) efficiently killed neuroblastoma cell lines carrying wildtype ALK (SK-N-BE(2)-C, IMR5/75), amplified ALK (NB-1), and those carrying the activating ALK F1174L mutation (Kelly), and, in cells carrying the activating R1275Q mutation (LAN-5), combination treatment decreased viable cell count.
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29515255 |
2018 |
rs863225281
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|
|
0.100 |
GeneticVariation |
BEFREE |
Accordingly, the combination of the ALK/MET inhibitor crizotinib and selective HDAC8 inhibitors (3-6 µM PCI-34051 or 10 µM 20a) efficiently killed neuroblastoma cell lines carrying wildtype ALK (SK-N-BE(2)-C, IMR5/75), amplified ALK (NB-1), and those carrying the activating ALK F1174L mutation (Kelly), and, in cells carrying the activating R1275Q mutation (LAN-5), combination treatment decreased viable cell count.
|
29515255 |
2018 |
rs113994087
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Accordingly, the combination of the ALK/MET inhibitor crizotinib and selective HDAC8 inhibitors (3-6 µM PCI-34051 or 10 µM 20a) efficiently killed neuroblastoma cell lines carrying wildtype ALK (SK-N-BE(2)-C, IMR5/75), amplified ALK (NB-1), and those carrying the activating ALK F1174L mutation (Kelly), and, in cells carrying the activating R1275Q mutation (LAN-5), combination treatment decreased viable cell count.
|
29515255 |
2018 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
Activating mutations within the full-length ALK kinase domain, most commonly R1275Q and F1174L, which play a major role in neuroblastoma, were recently identified.
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20632993 |
2010 |
rs863225281
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|
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0.100 |
GeneticVariation |
BEFREE |
Activating mutations within the full-length ALK kinase domain, most commonly R1275Q and F1174L, which play a major role in neuroblastoma, were recently identified.
|
20632993 |
2010 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
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26616860 |
2016 |
rs863225281
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|
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0.100 |
GeneticVariation |
BEFREE |
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
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26616860 |
2016 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
Altogether, we report for the first time that the expression of the human ALK-F1174L mutation in NCCs during embryonic development profoundly disturbs early sympathetic progenitor differentiation, in addition to increasing their proliferation, both mechanisms being potential crucial events in NB oncogenesis.
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31058082 |
2019 |
rs863225281
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0.100 |
GeneticVariation |
BEFREE |
Altogether, we report for the first time that the expression of the human ALK-F1174L mutation in NCCs during embryonic development profoundly disturbs early sympathetic progenitor differentiation, in addition to increasing their proliferation, both mechanisms being potential crucial events in NB oncogenesis.
|
31058082 |
2019 |
rs113994087
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0.100 |
GeneticVariation |
BEFREE |
Combined treatment with alectinib and vorinostat might be a novel therapeutic option for NB harboring the ALK R1275Q mutation.
|
31262882 |
2019 |
rs281864719
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|
0.100 |
GeneticVariation |
BEFREE |
Furthermore, two human neuroblastoma cell lines harbouring the F1174L</span> mutation were also sensitive to the inhibitor.
|
18923525 |
2008 |
rs863225281
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0.100 |
GeneticVariation |
BEFREE |
Furthermore, two human neuroblastoma cell lines harbouring the F1174L</span> mutation were also sensitive to the inhibitor.
|
18923525 |
2008 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
Here we present the evidence that murine neural crest progenitor cells can give rise to neuroblastoma upon transformation with MYCN or ALK(F1174L).
|
22484425 |
2013 |
rs863225281
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0.100 |
GeneticVariation |
BEFREE |
Here we present the evidence that murine neural crest progenitor cells can give rise to neuroblastoma upon transformation with MYCN or ALK(F1174L).
|
22484425 |
2013 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
Here, we report similar basal patterns of ALK phosphorylation between the neuroblastoma IMR-32 cell line, which expresses only the wild-type receptor (ALK(WT)), and the SH-SY5Y cell line, which exhibits a heterozygous ALK F1174L mutation and expresses both ALK(WT) and ALK(F1174L) receptors.
|
22479414 |
2012 |
rs863225281
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0.100 |
GeneticVariation |
BEFREE |
Here, we report similar basal patterns of ALK phosphorylation between the neuroblastoma IMR-32 cell line, which expresses only the wild-type receptor (ALK(WT)), and the SH-SY5Y cell line, which exhibits a heterozygous ALK F1174L mutation and expresses both ALK(WT) and ALK(F1174L) receptors.
|
22479414 |
2012 |
rs113994087
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0.100 |
GeneticVariation |
BEFREE |
Herein, we have illustrated the dynamic conformational property of wild-type ALK as well as the kinase activation equilibrium variation induced by two neuroblastoma mutations (R1275Q and Y1278S) and ATP binding by performing enhanced sampling accelerated Molecular Dynamics (aMD) simulations.
|
29638111 |
2018 |
rs863225285
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|
0.020 |
GeneticVariation |
BEFREE |
Herein, we have illustrated the dynamic conformational property of wild-type ALK as well as the kinase activation equilibrium variation induced by two neuroblastoma mutations (R1275Q and Y1278S) and ATP binding by performing enhanced sampling accelerated Molecular Dynamics (aMD) simulations.
|
29638111 |
2018 |
rs281864719
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0.100 |
GeneticVariation |
BEFREE |
However, lethal neuroblastoma</span> frequently developed in mice co-expressing ALK F1174L and MYCN, even in a genetic background where MYCN alone does not cause overt tumors.
|
31218818 |
2019 |
rs863225281
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0.100 |
GeneticVariation |
BEFREE |
However, lethal neuroblastoma</span> frequently developed in mice co-expressing ALK F1174L and MYCN, even in a genetic background where MYCN alone does not cause overt tumors.
|
31218818 |
2019 |
rs281864719
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|
0.100 |
GeneticVariation |
BEFREE |
Intrinsic susceptibility-MRI could thus potentially provide a non-invasive and clinically-exploitable method to help identifying children with MYCN-driven neuroblastoma harboring the ALK(F1174L) mutation at the time of diagnosis.
|
24667968 |
2014 |
rs863225281
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|
0.100 |
GeneticVariation |
BEFREE |
Intrinsic susceptibility-MRI could thus potentially provide a non-invasive and clinically-exploitable method to help identifying children with MYCN-driven neuroblastoma harboring the ALK(F1174L) mutation at the time of diagnosis.
|
24667968 |
2014 |