Targeting MYCN: a good BET for improving neuroblastoma therapy?

Cancer Discov. 2013 Mar;3(3):255-7. doi: 10.1158/2159-8290.CD-13-0018.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Animals
  • Cell Cycle Proteins
  • Female
  • Humans
  • N-Myc Proto-Oncogene Protein
  • Neuroblastoma / drug therapy*
  • Nuclear Proteins / antagonists & inhibitors*
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism*
  • Oncogene Proteins / genetics*
  • Transcription Factors / antagonists & inhibitors*
  • Transcription Factors / metabolism*

Substances

  • BRD4 protein, human
  • Cell Cycle Proteins
  • MYCN protein, human
  • N-Myc Proto-Oncogene Protein
  • Nuclear Proteins
  • Oncogene Proteins
  • Transcription Factors