Long-term effects of systemic cancer treatment on DNA oxidative damage: the potential for targeted therapies

Cancer Lett. 2012 Dec 31;327(1-2):134-41. doi: 10.1016/j.canlet.2011.12.029. Epub 2012 Jan 24.

Abstract

The main pathological consequence of free radical exposure is DNA damage, which is known to induce cell transformation and to facilitate important mutations in cancer progression. It is a matter of intense discussion whether the drug-induced production of free radicals limits the therapeutic efficacy of chemotherapeutics and enhances their toxicity or whether they may be enhanced to provoke cancer cell apoptosis. This paper reviews essential molecular processes to better understand the controversial role of free radicals in cancer development and progression, and discusses some novel therapeutic strategies based on oxidative stress induction and prevention.

Publication types

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

MeSH terms

  • Animals
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / therapeutic use*
  • Antioxidants / administration & dosage
  • Antioxidants / adverse effects
  • Antioxidants / therapeutic use*
  • Apoptosis / drug effects
  • DNA Damage / drug effects*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Molecular Targeted Therapy
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Oxidative Stress / drug effects*
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / drug effects
  • Time Factors

Substances

  • Antineoplastic Agents
  • Antioxidants
  • Reactive Oxygen Species