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 |
NEUROBLASTOMA, SUSCEPTIBILITY TO
|
|
0.700 |
CausalMutation
|
CLINVAR |
Differential inhibitor sensitivity of anaplastic lymphoma kinase variants found in neuroblastoma.
|
22072639 |
2011 |
Neuroblastoma
|
|
0.100 |
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 |
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 |
Adenocarcinoma of lung (disorder)
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Furthermore, HSP90 inhibition, as well as the second-generation ALK inhibitor TAE684, demonstrated activity in newly developed lung adenocarcinoma models driven by crizotinib-insensitive EML4-ALK L1196M or F1174L.
|
24327273 |
2014 |
Adenocarcinoma of lung (disorder)
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Furthermore, HSP90 inhibition, as well as the second-generation ALK inhibitor TAE684, demonstrated activity in newly developed lung adenocarcinoma models driven by crizotinib-insensitive EML4-ALK L1196M or F1174L.
|
24327273 |
2014 |
Childhood Neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Furthermore, two human neuroblastoma cell lines harbouring the F1174L</span> mutation were also sensitive to the inhibitor.
|
18923525 |
2008 |
Central neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Furthermore, two human neuroblastoma cell lines harbouring the F1174L</span> mutation were also sensitive to the inhibitor.
|
18923525 |
2008 |
Neuroblastoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Furthermore, two human neuroblastoma cell lines harbouring the F1174L</span> mutation were also sensitive to the inhibitor.
|
18923525 |
2008 |
Central neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
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 |
Central neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
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 |
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, SUSCEPTIBILITY TO
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
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 |
Central neuroblastoma
|
|
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 |
Neuroblastoma
|
|
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 |
Childhood Neuroblastoma
|
|
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 |
Adenocarcinoma of lung (disorder)
|
|
0.700 |
GeneticVariation
|
CLINVAR |
Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers.
|
22277784 |
2012 |