DNA damage and repair measured by comet assay in cancer patients
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
31421745
DOI
10.1016/j.mrgentox.2019.05.009
PII: S1383-5718(18)30345-0
Knihovny.cz E-resources
- Keywords
- Cancer aetiology, Cancer prognosis, Comet assay, DNA damage, DNA repair, Therapy prediction,
- MeSH
- Cost-Benefit Analysis MeSH
- DNA blood MeSH
- Epithelial Cells chemistry MeSH
- Carcinoma genetics metabolism MeSH
- Comet Assay * economics methods MeSH
- Hydrogen-Ion Concentration MeSH
- Blood Cells chemistry MeSH
- Humans MeSH
- Melanoma genetics metabolism MeSH
- Drug Monitoring methods MeSH
- Neoplasms genetics metabolism therapy MeSH
- DNA Repair * MeSH
- Organ Specificity MeSH
- DNA Damage * MeSH
- Sensitivity and Specificity MeSH
- Spermatozoa chemistry MeSH
- DNA Breaks MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- DNA MeSH
The last decade witnessed an increase in the use of comet assay for DNA damage monitoring in cancer patients and controls. Apart from case-control studies, reports described the determination of DNA damage prior to (baseline value) and after chemo-/radiotherapy, the treatment resulted in significantly elevated DNA damage. However, studies on DNA damage as a factor reflecting cancer prognosis and therapy prediction are scarce. In most cases, DNA damage was analysed in surrogate tissues. The data on DNA damage are available for 17 types of cancer. The reviewed data unambiguously pinpoint the usefulness of the comet assay in human cancer research due to its sensitivity and cost-effectiveness in evaluating DNA damage associated with the disease and with the treatment. DNA repair capacity (DRC) represents a complex marker for functional evaluation of multigene DNA repair processes in cancer onset with future prospects in personalized prevention and/or cancer treatment. A comparison between studies and more general conclusions are precluded by a variable design of the studies and a lack of standard protocol for both DNA damage and DRC determination. Since cancer is a heterogeneous complex disease, numerous points have to be considered: a) DNA damage and DRC measured in surrogate/target tissues, b) changes in the levels of DNA damage and DRC may be a cause or a consequence of the disease, c) changes in DRC alter sensitivity of tumour cells to antineoplastic drugs, d) one time point-sampling of patients provides insufficient information on the role of DNA damage and its repair in carcinogenesis. Finally, systemic cancer therapy is targeted at DNA damage and its repair. A proper understanding of these processes is a key precondition for the optimisation of therapy regimens, prediction of therapeutic response and prognosis in cancer patients.
References provided by Crossref.org
Editorial: Current understanding of genomic and chromosomal instabilities in solid malignancies
DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome