Neuroblastoma recurrent
|
|
0.010 |
GeneticVariation
|
BEFREE |
In one patient with relapsed neuroblastoma with ALK F1174L mutation and ALK amplification, lorlatinib was used in a compassionate use program, and it showed some efficacy.
|
31747416 |
2019 |
hereditary neuroblastoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
In this study, we show that the novel ALK inhibitor alectinib effectively suppressed cell proliferation and induces apoptosis in NB cell lines with either wild-type ALK or mutated ALK (F1174L and D1091N) by blocking ALK-mediated PI3K/Akt/mTOR signaling.
|
28455243 |
2017 |
Congenital chromosomal disease
|
|
0.010 |
GeneticVariation
|
BEFREE |
Targeted ALK(F1174L) and MYCN coexpression revealed a strong synergism in inducing neuroblastoma with minimal chromosomal aberrations, suggesting that fewer secondary hits are required for tumor induction if both oncoproteins are targeted.
|
22764207 |
2012 |
Inflammatory Myofibroblastic Tumor
|
|
0.010 |
GeneticVariation
|
BEFREE |
Here we report the identification of a secondary mutation in ALK, F1174L, as one cause of crizotinib resistance in a patient with an inflammatory myofibroblastic tumor (IMT) harboring a RANBP2-ALK translocation who progressed while on crizotinib therapy.
|
21030459 |
2010 |
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 |
Carcinogenesis
|
|
0.020 |
GeneticVariation
|
BEFREE |
The two most frequent mutations, ALK-F1174L and ALK-R1275Q, contribute to NB tumorigenesis in mouse models, and cooperate with MYCN in the oncogenic process.
|
24947326 |
2014 |
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 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
Next, we performed cross-species genomic analyses to identify commonly transcriptionally perturbed genes in MYCN/ALK(F1174L) double transgenic versus MYCN transgenic mouse tumors as compared with the mutant ALK-driven transcriptome in human neuroblastomas.
|
25805801 |
2015 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
While orthotopic implantations of MONC- 1 parental cells in nude mice generated various tumor types, such as NB, osteo/ chondrosarcoma, and undifferentiated tumors, due to v-Myc oncogenic activity, MONC-1-ALK-F1174L cells only produced undifferentiated tumors.
|
24947326 |
2014 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
We demonstrate that quantitation of the transverse relaxation rate R2* (s(-1)) using intrinsic susceptibility-MRI under baseline conditions and during hyperoxia, can robustly discriminate this differential vascular phenotype, and identify MYCN-driven tumors harboring the ALK(F1174L) mutation with high specificity and selectivity.
|
24667968 |
2014 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
Combined treatment with crizotinib and an ATP-competitive mTOR inhibitor abrogated RPS6 phosphorylation, leading to reduced tumor growth and prolonged survival in ALK(F1174L)/MYCN-positive models compared to single agent treatment.
|
25228590 |
2014 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
Expression of MYCN or ALK(F1174L), one of the oncogenic ALK variants identified in primary neuroblastomas, enabled these cells to grow independently of c-MycER(T) activity in vitro and caused formation of neuroblastoma-like tumors in vivo in contrast to parental JoMa1 cells and JoMa1 cells-expressing TrkA or GFP.
|
22484425 |
2013 |
Neoplasms
|
|
0.080 |
GeneticVariation
|
BEFREE |
Targeted ALK(F1174L</span>) and MYCN coexpression revealed a strong synergism in inducing neuroblastoma with minimal chromosomal aberrations, suggesting that fewer secondary hits are required for tumor induction if both oncoproteins are targeted.
|
22764207 |
2012 |
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 |
Central neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
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 |
Childhood Neuroblastoma
|
|
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 |
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 |
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 |