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Expression of EWS-ETS fusions in NIH3T3 cells reveals significant differences to Ewing's sarcoma
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EWS-FLI1 fusion protein up-regulates critical genes in neural crest development and is responsible for the observed phenotype of Ewing's family of tumors
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Ewing sarcomas with p53 mutation or p16/p14ARF homozygous deletion:: A highly lethal subset associated with poor chemoresponse
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EWS/FLI function varies in different cellular backgrounds
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The Ewing's sarcoma oncoprotein EWS/FLI induces a p53-dependent growth arrest in primary human fibroblasts
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Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation
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