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A qPCR-Based Assay to Quantify Oxidized Guanine and Other FPG-Sensitive Base Lesions within Telomeric DNA


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Telomere shortening is an important risk factor for cancer and accelerated aging. However, it is becoming evident that oxidatively damaged DNA within the telomere sequence may also cause telomere dysfunction.

The number of telomeric repeats decreases with each cell division in somatic cells, and this process is accelerated as a result of base damage or strand breaks induced within the telomere sequence. Excessively short telomeres have been shown to lead to chromosomal instability via telomere end-fusion and the generation of breakage-fusion-bridge cycles.

These changes in genome stability are important initiating events in aging-related disorders such as cancer. Furthermore, there is increasing evidence that telomere shortening and dysfunction are associated with obesity, psychological stress, immune dysregulation, cancer, cardiovascular disease, and neurodegenerative disorders such as Alzheimer disease. In telomeres, guanine is particularly sensitive to oxidation, and strand breaks within the telomere sequence leads to accelerated telomere shortening.

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