Intrinsic tumour suppression

Nature. 2004 Nov 18;432(7015):307-15. doi: 10.1038/nature03098.


Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis*
  • Drug Resistance, Neoplasm
  • Humans
  • Neoplasms / genetics
  • Neoplasms / pathology*
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism*
  • Tumor Suppressor Protein p53 / metabolism


  • Oncogene Proteins
  • Tumor Suppressor Protein p53