Evidence that c-myc mediated apoptosis does not require wild-type p53 during lymphomagenesis

Oncogene. 1995 Jul 6;11(1):175-9.


Deregulation of c-myc, frequently implicated in oncogenesis, is associated with increased cell proliferation and also cell death. Similarly, the p53 tumor suppressor gene commonly mutated in human tumors, is known to induce apoptosis or cell cycle arrest in its wild-type conformation. Genetically altered mice simultaneously overexpressing c-myc and possessing a disrupted p53 gene were used to investigate whether c-myc mediated apoptosis requires wild-type p53. The accelerated development of malignant lymphomas in these mice was found to be a consequence of enhanced proliferation and not reduced apoptosis resulting from the synergistic effect of c-myc overexpression and p53 inactivation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alleles
  • Animals
  • Apoptosis / genetics*
  • Base Sequence
  • Cell Division / genetics
  • Chromosome Deletion
  • DNA Primers
  • Genes, myc*
  • Genes, p53*
  • Heterozygote
  • Lymphoma / genetics*
  • Lymphoma / pathology
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data


  • DNA Primers