title: Parsing Myc Paralogs in Oncogenesis.
abstract: Myc and its paralog MycN are thought to be functionally redundant, but Myc- and MycN-driven medulloblastomas exhibit distinct phenotypes. In this issue of Cancer Cell, Vo and colleagues (2016) show that this phenotypic difference stems from the preferential ability of Myc, relative to MycN, to bind Miz1 and repress transcription.
authors.affiliation: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
authors.forename: Haritha
authors.initials: H
authors.lastname: Mathsyaraja
authors.affiliation: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Electronic address: eisenman@fhcrc.org.
authors.forename: Robert N
authors.initials: RN
authors.lastname: Eisenman
mesh_terms: D000818:Animals; D002528:Cerebellar Neoplasms / Q000378:metabolism* / Q000473:pathology*; D008527:Medulloblastoma / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D050828:Protein Inhibitors of Activated STAT / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism*
chemical_list: D009687:Nuclear Proteins; D050828:Protein Inhibitors of Activated STAT; D016271:Proto-Oncogene Proteins c-myc