Oxidatively induced DNA damage is caused by endogenous and exogenous sources in living organisms. Many resulting DNA lesions are mutagenic and lead to mutations commonly found in cancer. Repairs mechanisms exist to repair this type of DNA damage. Unrepaired and accumulated DNA lesions may lead to carcinogenesis and other disease processes. Defects in DNA repair are associated with cancer. Oxidatively induced DNA lesions accumulate in cancerous tissues, possibly contributing to genomic instability and metastatic potential. Recent evidence suggests that some tumors may even possess increased DNA repair capacity, leading to therapy resistance. DNA repair inhibitors are being developed to target the repair pathways and increase the efficacy of cancer therapy. Oxidatively induced DNA lesions and DNA repair proteins are potential biomarkers for early detection, cancer risk assessment, prognosis and monitoring the therapy. Overall, accumulated evidence suggests that oxidatively induced DNA damage and its repair are important factors in carcinogenesis, and deserves more research to understand and fight cancer.
Citation: Journal of Molecular Biomarkers & Diagnosis
Pub Type: Journals
DNA repair, DNA repair proteins, human OGG1, LC-MS/MS, stable isotope-labeling, labeled internal standards, thaliana, Candida albicans