title: Multiple functions of a glioblastoma fusion oncogene.
abstract: RNA sequencing facilitates the discovery of novel gene fusions in cancer. In this issue of the JCI, Parker et al. identify an FGFR3-TACC3 fusion oncogene in glioblastoma and demonstrate a novel mechanism of pathogenicity. A miR-99a binding site within the 3'-untranslated region (3'-UTR) of FGFR3 is lost, releasing FGFR3 signaling from miR-99a-dependent inhibition and greatly enhancing tumor progression relative to WT FGFR3. These results provide compelling insight into the pathogenicity of a novel fusion oncogene and suggest new therapeutic approaches for a subset of glioblastomas.
authors.affiliation: Ludwig Institute for Cancer Research, UCSD, La Jolla, California, USA.
authors.forename: Ivan
authors.initials: I
authors.lastname: Babic
authors.forename: Paul S
authors.initials: PS
authors.lastname: Mischel
mesh_terms: D000818:Animals; D001932:Brain Neoplasms / Q000235:genetics*; D050939:Gene Fusion; D005909:Glioblastoma / Q000235:genetics*; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D008869:Microtubule-Associated Proteins / Q000235:genetics*; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics*
chemical_list: C561679:MIRN99 microRNA, human; D035683:MicroRNAs; D008869:Microtubule-Associated Proteins; C120551:TACC3 protein, human; C496365:FGFR3 protein, human; D051498:Receptor, Fibroblast Growth Factor, Type 3