Journal
CANCER CELL
Volume 25, Issue 1, Pages 12-19Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2013.12.005
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Funding
- Cancer Institute New South Wales (CINSW)
- Glenn Foundation for Medical Research
- Juvenile Diabetes Research Foundation
- United Mitochondrial Disease Foundation
- National Health and Medical Research Council of Australia
- National Institutes of Health
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Why does cancer risk increase as we age? Frequently attributed to the multi-hit hypothesis and the time required to accumulate genomic mutations, this question is a matter of ongoing debate. Here, we propose that the normal decline in oxidative metabolism during aging constitutes an early and important hit that drives tumorigenesis. Central to these metabolic changes are the sirtuins, a family of NAD(+)-dependent deacylases that have evolved as coordinators of physiological responses to nutrient intake and energetic demand. Thus, the modulation of sirtuins might be a fruitful approach to reversing the age-related metabolic changes that could underlie tumorigenesis.
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