title: When deletions gain functions: commandeering epigenetic mechanisms.
abstract: Recurrent chromosomal deletions in cancer are typically thought to harbor tumor suppressors. In a recent publication in Nature, Northcott and colleagues identify a novel region of structural variation in medulloblastoma that leads to oncogenic activation of GFI1B and GFI1 by repositioning these genes next to super-enhancers.
authors.affiliation: Departments of Neurology, Pediatrics, Neurosurgery, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA.
authors.forename: Justin
authors.initials: J
authors.lastname: Chen
authors.affiliation: Departments of Neurology, Pediatrics, Neurosurgery, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: waweiss@gmail.com.
authors.forename: William A
authors.initials: WA
authors.lastname: Weiss
mesh_terms: D000818:Animals; D004268:DNA-Binding Proteins / Q000235:genetics*; D004742:Enhancer Elements, Genetic / Q000235:genetics*; D056914:Genomic Structural Variation / Q000235:genetics*; D006801:Humans; D008527:Medulloblastoma / Q000235:genetics*; D009857:Oncogenes / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D012097:Repressor Proteins / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D014157:Transcription Factors