When deletions gain functions: commandeering epigenetic mechanisms

Justin Chen; William A Weiss

doi:10.1016/j.ccr.2014.07.021

When deletions gain functions: commandeering epigenetic mechanisms

Cancer Cell. 2014 Aug 11;26(2):160-1. doi: 10.1016/j.ccr.2014.07.021.

Authors

Justin Chen¹, William A Weiss²

Affiliations

¹ Departments of Neurology, Pediatrics, Neurosurgery, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA.
² 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.

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.

Publication types

Comment

MeSH terms

Animals
DNA-Binding Proteins / genetics*
Enhancer Elements, Genetic / genetics*
Genomic Structural Variation / genetics*
Humans
Medulloblastoma / genetics*
Oncogenes / genetics*
Proto-Oncogene Proteins / genetics*
Repressor Proteins / genetics*
Transcription Factors / genetics*

Substances

DNA-Binding Proteins
Proto-Oncogene Proteins
Repressor Proteins
Transcription Factors

Abstract

Publication types

MeSH terms

Substances

Grants and funding