|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Oncogenesis of Ewing sarcoma (EwS), the second most common malignant bone tumor of childhood and adolescence, is dependent on the expression of chimeric EWSR1-ETS fusion oncogenes, most often EWSR1-FLI1 (E/F).
|
31811703 |
2020 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In addition to regulating transcription, EWS-FLI1 also alters the splicing of many mRNA isoforms, but the role of splicing modulation in ES oncogenesis is not well understood.
|
31392992 |
2019 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
1008-1019) explore the ability of GGAA repeats to act as alternative enhancers activated by EWS-FLI1 in Ewing sarcoma and contribute to tumorigenesis.
|
30068701 |
2018 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
EWS-FLI1 is an aberrant transcription factor driving Ewing sarcoma tumorigenesis by either transcriptionally inducing or repressing specific target genes.
|
27375017 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Although EWS-FLI1 is specific for cancer cells, and required for tumorigenesis, directly targeting this transcription factor has proven challenging.
|
27557498 |
2016 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In Ewing sarcoma (EWS) both CD99 and EWS-FLI1 concur to oncogenesis and inhibition of differentiation.
|
26616853 |
2016 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
EWS-FLI1 modulation of mRNA splicing may provide insight into the contribution of splicing toward oncogenesis, and, reciprocally, EWS-FLI1 interactions with splicing proteins may inform the splicing code.
|
25737553 |
2015 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Although EWS/FLI-1 chimeric proteins are necessary for carcinogenesis, additional events seem to be required for transformation to occur.
|
23831569 |
2014 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
The functional role of endogenous EWS at stem cell level on both senescence and tumorigenesis is a link between cancer and aging.
|
24294922 |
2014 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
This is the first study to detect a specific fusion gene in mesothelioma (the reason how frequent the EWSR1-YY1 fusion is remains uncertain) and also the first time that direct involvement of YY1 in oncogenesis has been demonstrated.
|
23630070 |
2013 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
However, expression of the EWS/FLI-1 chimeric oncogene by itself is insufficient for carcinogenesis, suggesting that additional events are required.
|
22241085 |
2012 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The incidence of tumors increased in a p53 mutant background, suggesting that the p53 pathway suppresses EWS-FLI1-driven tumorigenesis.
|
21979944 |
2012 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
FUS, EWSR1 and TAF15, constituting the FET protein family, are abundant, highly conserved RNA-binding proteins with important roles in oncogenesis and neuronal disease, yet their RNA targets and recognition elements are unknown.
|
22081015 |
2011 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
It is proposed that EWSR1-hSNF2H may act as an oncogenic chromatin-remodeling factor and that its expression contributes to Ewing sarcoma/primitive neuroectodermal tumorigenesis.
|
21113140 |
2011 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Evaluation of existing data on the known EWSR1-POU5F1 tumors suggests that the fusion gene functions in a wide variety of cell types and may modify the differentiation state of cells, resulting in susceptibility to tumorigenesis.
|
21962892 |
2011 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To clarify the roles of the EWS-POU5F1 chimera in tumorigenesis and tumor cell maintenance, we used small-interfering RNA-mediated gene silencing.
|
20203285 |
2010 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
EWS/Fli-1 is considered to be a transcriptional activator and to play a significant role in tumorigenesis of Ewing's sarcoma.
|
19642105 |
2010 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results might provide new insight into the oncogenesis of EFTs by EWS-Fli1 via the inhibition of p53 function.
|
20153576 |
2010 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Therefore, understanding the protein-protein interactions of EWS-FLI1 and the pathways that are regulated by these partnerships will inform both oncogenesis and therapeutics.
|
20547696 |
2010 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
EWS/FLI and its downstream target NR0B1 interact directly to modulate transcription and oncogenesis in Ewing's sarcoma.
|
19920188 |
2009 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
How the new fusion gene contributes to tumorigenesis is unknown, but the finding of an EWSR1 rearrangement suggests that this, possibly even the EWSR1-ZNF444, is a defining pathogenetic feature of at least a subset of these tumors.
|
19760602 |
2009 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our data link EWS-FLI1 to the NOTCH and p53 pathways and provide a plausible basis both for NOTCH tumor suppressor effects and oncogenesis of cancers that retain wild-type p53.
|
18757425 |
2008 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
(1-5) EWS-FLI is an oncogenic transcription factor that regulates genes involved in tumorigenesis.
|
18256529 |
2008 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
However, the specific details of EWS/PNET oncogenesis and exact role of EWS-FLI1 remain largely unknown.
|
18622580 |
2008 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Gene expression profile analysis demonstrated that about 10% of the genes regulated by EWS/FLI1 in Ewing's cells are DAX1 targets, confirming the importance of DAX1 in Ewing's oncogenesis.
|
18591936 |
2008 |