Cellular senescence in cancer treatment: friend or foe?

J Clin Invest. 2004 Jan;113(2):169-74. doi: 10.1172/JCI20784.


Damage to DNA, the prime target of anticancer therapy, triggers programmed cellular responses. In addition to apoptosis, therapy-mediated premature senescence has been identified as another drug-responsive program that impacts the outcome of cancer therapy. Here, we discuss whether induction of senescence is a beneficial or, rather, a detrimental consequence of the therapeutic intervention.

Publication types

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

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis
  • Cell Line, Tumor
  • Cellular Senescence*
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • DNA / metabolism
  • DNA Damage
  • Humans
  • Models, Biological
  • Neoplasms / pathology*
  • Neoplasms / therapy*
  • Tumor Suppressor Protein p53 / metabolism


  • Antineoplastic Agents
  • Cyclin-Dependent Kinase Inhibitor p16
  • Tumor Suppressor Protein p53
  • DNA