c-Myc, genome instability, and tumorigenesis: the devil is in the details

Curr Top Microbiol Immunol. 2006;302:169-203. doi: 10.1007/3-540-32952-8_7.

Abstract

The c-myc oncogene acts as a pluripotent modulator of transcription during normal cell growth and proliferation. Deregulated c-myc activity in cancer can lead to excessive activation of its downstream pathways, and may also stimulate changes in gene expression and cellular signaling that are not observed under non-pathological conditions. Under certain conditions, aberrant c-myc activity is associated with the appearance of DNA damage-associated markers and karyotypic abnormalities. In this chapter, we discuss mechanisms by which c-myc may be directly or indirectly associated with the induction of genomic instability. The degree to which c-myc-induced genomic instability influences the initiation or progression of cancer is likely to depend on other factors, which are discussed herein.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Cycle
  • DNA Damage
  • DNA Repair
  • Gene Expression Regulation
  • Genes, myc*
  • Genomic Instability*
  • Humans
  • Models, Biological
  • Neoplasms / etiology*
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Oncogenes
  • Oncogenic Viruses / pathogenicity
  • Reactive Oxygen Species / metabolism

Substances

  • Reactive Oxygen Species