c-Myc dependent initiation of genomic instability during neoplastic transformation

Curr Top Microbiol Immunol. 1997:224:201-7. doi: 10.1007/978-3-642-60801-8_20.

Abstract

The dihydrofolate reductase (DHFR) gene is a target of c-Myc in genomic instability. The induced overexpression of c-Myc in cell lines is followed by the amplification and rearrangement of the DHFR gene. Furthermore, the constitutive upregulation of c-Myc protein coincides with genomic instability of the DHFR gene in lymphoid, non-lymphoid and in tumor lines. The amplification of the DHFR gene is locus-specific and independent of species origins. We have now addressed the question whether inducible deregulation of c-Myc is followed by DHFR gene amplification in vivo. We show that the DHFR gene is a target of c-Myc-dependent neoplasia in vivo and propose a role for genomic instability during the initiation of neoplastic transformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinogens / toxicity
  • Cell Transformation, Neoplastic / drug effects
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Neoplastic / metabolism*
  • Gene Amplification
  • In Situ Hybridization, Fluorescence
  • Mice
  • Mice, Inbred BALB C
  • Models, Biological
  • Plasmacytoma / chemically induced
  • Plasmacytoma / genetics
  • Plasmacytoma / metabolism
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Terpenes / toxicity
  • Tetrahydrofolate Dehydrogenase / genetics

Substances

  • Carcinogens
  • Proto-Oncogene Proteins c-myc
  • Terpenes
  • pristane
  • Tetrahydrofolate Dehydrogenase