The role of DNA damage and repair in toxicity to postmitotic cells caused by cancer therapies

M. R. Vasko, B. Shariati, N. Zanville

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations


With increased survival rates for cancer patients, toxicity secondary to anticancer therapies has become a prevalent clinical concern. Of major importance are toxicities occurring in postmitotic cells (cardiac muscle, skeletal muscle, and neurons) since these toxicities are quite debilitating, they often persist long after therapy is discontinued, and few interventions exist to prevent or reverse them. Although the mechanisms mediating these toxicities are not known, one promising area that requires further exploration is the ability of DNA repair mechanisms to reverse the toxic effects of a number of anticancer drugs. For example, studies in animal models show that enhancing the base excision repair pathway attenuates neuronal damage by chemotherapeutic agents, suggesting that manipulating DNA repair mechanisms may be a novel approach to diminish neurotoxicity during or after cancer therapy. Whether DNA damage and repair are critical in cardiac and skeletal muscle toxicity after cancer therapy remains to be determined.

Original languageEnglish (US)
Title of host publicationDNA Repair in Cancer Therapy
Subtitle of host publicationMolecular Targets and Clinical Applications: Second Edition
PublisherElsevier Inc.
Number of pages46
ISBN (Print)9780128035825
StatePublished - Jun 21 2016



  • Base excision repair
  • Cardiotoxicity
  • Chemotherapy-induced peripheral neuropathy
  • Cognitive dysfunction
  • DNA damage
  • Myopathy
  • Nucleotide excision repair
  • Ototoxicity

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Vasko, M. R., Shariati, B., & Zanville, N. (2016). The role of DNA damage and repair in toxicity to postmitotic cells caused by cancer therapies. In DNA Repair in Cancer Therapy: Molecular Targets and Clinical Applications: Second Edition (pp. 383-428). Elsevier Inc..