title: Targeting MYCN: a good BET for improving neuroblastoma therapy?
abstract: Direct targeting of oncogenic MYC proteins has been an elusive goal of many cancer drug development efforts. In this issue of Cancer Discovery, Stegmaier and colleagues demonstrate that pharmacologically interfering with the bromodomain and extraterminal (BET) class of proteins potently depletes MYCN in neuroblastoma cells, resulting in cellular cytotoxicity and thus providing a novel approach with a potential impact on a previously undruggable major oncogene.
authors.affiliation: Division of Oncology and the Center for Childhood Cancer Research. The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.
authors.forename: Robert W
authors.initials: RW
authors.lastname: Schnepp
authors.forename: John M
authors.initials: JM
authors.lastname: Maris
mesh_terms: D000818:Animals; D018797:Cell Cycle Proteins; D005260:Female; D006801:Humans; D000071447:N-Myc Proto-Oncogene Protein; D009447:Neuroblastoma / Q000188:drug therapy*; D009687:Nuclear Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics* / Q000378:metabolism*; D015513:Oncogene Proteins / Q000235:genetics*; D014157:Transcription Factors / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D000092468:Bromodomain Containing Proteins
chemical_list: D018797:Cell Cycle Proteins; D000071447:N-Myc Proto-Oncogene Protein; D009687:Nuclear Proteins; D015513:Oncogene Proteins; D014157:Transcription Factors; C441289:BRD4 protein, human; D000092468:Bromodomain Containing Proteins; C459801:MYCN protein, human