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lüll Oncogenic partnerships: EWS-FLI1 protein interactions initiate key pathways of Ewing s sarcoma Erkizan HV; Uversky VN; Toretsky JAClin Cancer Res 2010[Aug]; 16 (16): 4077-83Targeted therapy for cancer, which is specifically directed toward the cancer without any potential for effects outside of controlling the tumor, is a gold standard for treatment. Ewing's sarcoma contains the potential target EWS-FLI1, as a result of a pathognomonic chromosomal translocation. The EWS-FLI1 fusion protein includes the EWS domain, a potent transcriptional activator alongside the highly conserved FLI1 ets DNA-binding domain. Because of the combination of these domains, the EWS-FLI1 fusion protein acts as an aberrant transcription factor whose expression results in cellular transformation. EWS-FLI1 functions by binding to normal cellular protein partners in transcription and splicing, similar to how a virus would corrupt normal cellular machinery for virion production. Therefore, understanding the protein-protein interactions of EWS-FLI1 and the pathways that are regulated by these partnerships will inform both oncogenesis and therapeutics. This review describes the known protein partners and transcriptional targets of EWS-FLI1, while proposing strategies for exploiting these partnerships with targeted therapy.|Animals[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Humans[MESH]|Oncogene Proteins, Fusion/*genetics/metabolism[MESH]|Proto-Oncogene Protein c-fli-1[MESH]|RNA-Binding Protein EWS[MESH]|Sarcoma, Ewing/*genetics/*metabolism/pathology[MESH]|Signal Transduction/physiology[MESH]|Transcription Factors/*genetics/metabolism[MESH]|Transcription, Genetic[MESH]|Translocation, Genetic[MESH] |