Journal
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 7
Volume 7, Issue -, Pages 145-159Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-011110-130237
Keywords
EWS-FLI1; oncogenesis; chromosomal translocation; transcription; chromatin immunoprecipitation; stem cells
Categories
Funding
- NCI NIH HHS [P30-CA042014, R01 CA140394, P01 CA106450, R21 CA138295, R01CA140394, P30 CA042014] Funding Source: Medline
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Approximately one-third of sarcomas contain specific translocations. Ewing sarcoma is the prototypical member of this group of sarcomas; it was the first to be recognized pathologically as a singular entity and to have its signature translocation defined cytogenetically, which led to the identification of its key driver alteration, the EWS-FLI1 gene fusion that encodes this aberrant, chimeric transcription factor. We review recent progress in selected areas of Ewing sarcoma research, including the application of genome-wide chromatin immunoprecipitation analyses, to provide a comprehensive view of the EWS-FLI1 target gene repertoire, the identification of EWS-FLI1 target genes that may also point to therapeutically targetable pathways, and data from model systems as they relate to the elusive cell of origin of Ewing sarcoma and its possible similarities to mesenchymal stem cells.
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