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Publication Citation: Oxidatively Induced DNA Damage and Cancer

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Author(s): M Miral Dizdar;
Title: Oxidatively Induced DNA Damage and Cancer
Published: December 31, 2012
Abstract: Endogenous and exogenous sources cause oxidatively induced DNA damage in living organisms by a variety of mechanisms. Resulting DNA lesions are mutagenic and, unless repaired, lead to a variety of mutations and consequently to genetic instability, which a hallmark of cancer. Oxidatively induced DNA damage is repaired in living cells by different pathways that involve a large number of proteins. Unrepaired and accumulated DNA lesions may lead to disease processes including carcinogenesis. Mutations also occur in DNA repair genes, destabilizing DNA repair system. A majority of cancer cell lines have somatic mutations in their DNA repair genes. In addition, polymorphisms in these genes constitute a risk factor for cancer. In general, defects in DNA repair are associated with cancer. Numerous DNA repair enzymes exist that possess different, but sometimes overlapping substrate specificities for removal of oxidatively induced DNA lesions. Recent evidence suggests that some type of tumors possess increased DNA repair capacity that may lead to therapy resistance. DNA repair pathways are drug targets to develop DNA repair inhibitors to increase the efficacy of cancer therapy. Oxidatively induced DNA lesions and DNA repair proteins may serve as potential biomarkers for early detection, cancer risk assessment, prognosis and monitoring the therapy. Taken together, a large body of accumulated evidence suggests that oxidatively induced DNA damage and its repair are important factors in development of human cancers. Thus this field deserves more research to contribute to the development of cancer biomarkers, DNA repair inhibitors and treatment approaches to better understand and fight cancer.
Citation: Cancer Letters
Issue: 327
Pages: pp. 26 - 47
Keywords: Cancer; DNA damage and repair; DNA repair defects; Cancer biomarkers
Research Areas: DNA
DOI: http://dx.doi.org/10.1016/j.canlet.2012.01.016  (Note: May link to a non-U.S. Government webpage)
PDF version: PDF Document Click here to retrieve PDF version of paper (2MB)