NEUROBLASTOMA, SUSCEPTIBILITY TO, 3
|
|
0.800 |
CausalMutation
|
CLINVAR |
|
|
|
NEUROBLASTOMA, SUSCEPTIBILITY TO, 3
|
|
0.800 |
CausalMutation
|
CLINVAR |
|
|
|
NEUROBLASTOMA, SUSCEPTIBILITY TO, 3
|
|
0.800 |
GeneticVariation
|
UNIPROT |
|
|
|
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 |
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 |
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 |
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 |
Neuroblastoma
|
|
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 |
Central neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Central neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
|
26616860 |
2016 |
Childhood Neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
|
26616860 |
2016 |
Neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
|
26616860 |
2016 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
ALK mutations conferring differential resistance to structurally diverse ALK inhibitors.
|
21948233 |
2011 |
Neoplasms
|
|
0.080 |
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 |
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 |
Neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Carcinogenesis
|
|
0.020 |
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 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
AZD3463 also exhibited significant therapeutic efficacy on the growth of the NB tumors with WT and F1174L activating mutation ALK in orthotopic xenograft mouse models.
|
26786851 |
2016 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant.
|
21575866 |
2011 |