Journal
CANCER RESEARCH
Volume 80, Issue 3, Pages 367-374Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-19-0924
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Funding
- NIH/NCI [R50CA233042, U01CA182940, U01CA199336]
- NIH [P30CA15704, UO1CA152756, R01CA194663, RO1CA220004, RO1189184, U54CA143862, P01CA077852]
- R.A.C.E. Charities
- Cottrell Family Fund [R03 CA165153, R01 CA112516, R01 CA114467, R01 CA120523, U24 CA074794]
- Listwin Family Foundation
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The incidence of cancer, adjusted for secular trends, is directly related to age, and advanced chronologic age is one of the most significant risk factors for cancer. Organismal aging is associated with changes at the molecular, cellular, and tissue levels and is affected by both genetic and environmental factors. The specific mechanisms through which these age-associated molecular changes contribute to the increased risk of aging-related disease, such as cancer, are incompletely understood. DNA methylation, a prominent epigenetic mark, also changes over a lifetime as part of an epigenetic aging process. Here, we give an update and review of epigenetic aging, in particular, the phenomena of epigenetic drift and epigenetic clock, with regard to its implication in cancer etiology. We discuss the discovery of the DNA methylationbased biomarkers for biological tissue age and the construction of various epigenetic age estimators for human clinical outcomes and health/life span. Recent studies in various types of cancer point to the significance of epigenetic aging in tumorigenesis and its potential use for cancer risk prediction. Future studies are needed to assess the potential clinical impact of strategies focused on lowering cancer risk by preventing premature aging or promoting healthy aging.
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