NEUROBLASTOMA, SUSCEPTIBILITY TO, 3
|
|
0.700 |
SusceptibilityMutation
|
CLINVAR |
|
|
|
NEUROBLASTOMA, SUSCEPTIBILITY TO, 3
|
|
0.700 |
CausalMutation
|
CLINVAR |
|
|
|
Central neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Central neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
Activating ALK mutations found in neuroblastoma are inhibited by Crizotinib and NVP-TAE684.
|
21838707 |
2011 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
Activating mutations in ALK provide a therapeutic target in neuroblastoma.
|
18923525 |
2008 |
Neoplasms
|
|
0.020 |
GeneticVariation
|
BEFREE |
ALK mutations occur in equal frequencies across all genomic subtypes, but F1174L mutants are observed in a higher frequency of MYCN-amplified tumors and show increased transforming capacity as compared with the R1275Q mutants.
|
20719933 |
2010 |
Central neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
Differential inhibitor sensitivity of anaplastic lymphoma kinase variants found in neuroblastoma.
|
22072639 |
2011 |
Brain Neoplasms
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Differential inhibitor sensitivity of anaplastic lymphoma kinase variants found in neuroblastoma.
|
22072639 |
2011 |
Primary malignant neoplasm
|
|
0.010 |
GeneticVariation
|
BEFREE |
Here, we employ a bioinformatics method, Prediction of T Cell Epitopes for Cancer Therapy, to analyze sequencing data from neuroblastoma patients and identify a recurrent anaplastic lymphoma kinase mutation (<i>ALK</i> R1275Q) that leads to two high affinity neoepitopes when expressed in complex with common HLA alleles.
|
29441070 |
2018 |
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
Here, we employ a bioinformatics method, Prediction of T Cell Epitopes for Cancer Therapy, to analyze sequencing data from neuroblastoma patients and identify a recurrent anaplastic lymphoma kinase mutation (<i>ALK</i> R1275Q) that leads to two high affinity neoepitopes when expressed in complex with common HLA alleles.
|
29441070 |
2018 |
Neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Central neuroblastoma
|
|
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 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
Mammary Neoplasms
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
Mammary Neoplasms
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |