title: ChIP-ping away at EWS/ETS transcription networks.
abstract: In this issue of Cancer Cell, Riggi and colleagues use a genomic approach to define two distinct molecular mechanisms through which the chimeric EWS/FLI1 oncoprotein regulates target genes in Ewing sarcoma, expanding a framework upon which to model the target gene network and test strategies for antagonizing growth of this tumor.
authors.affiliation: Division of Hematology/Oncology, Department of Pediatrics, Gwynne Hazen Cherry Memorial Laboratories, University of California, Los Angeles, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: cdenny@ucla.edu.
authors.forename: Christopher T
authors.initials: CT
authors.lastname: Denny
mesh_terms: D000818:Animals; D001859:Bone Neoplasms / Q000235:genetics*; D042002:Chromatin Assembly and Disassembly; D006801:Humans; D015514:Oncogene Proteins, Fusion / Q000502:physiology*; D051789:Proto-Oncogene Protein c-fli-1 / Q000502:physiology*; D034802:RNA-Binding Protein EWS / Q000502:physiology*; D012512:Sarcoma, Ewing / Q000235:genetics*
chemical_list: C106031:EWS-FLI fusion protein; D015514:Oncogene Proteins, Fusion; D051789:Proto-Oncogene Protein c-fli-1; D034802:RNA-Binding Protein EWS