The cancer-aging hypothesis suggests that the activation of some tumor suppressor mechanisms beneficially prevents cancer but also untowardly promotes mammalian aging. Along these lines, activation of tumor suppressor mechanisms that inhibit the cell cycle (e.g. p16(INK4a) and p53) in response to DNA damage and other age-promoting stimuli has taken center stage in immune-aging research. Immune cells are intrinsically susceptible to transforming events due to V(D)J recombination, a high rate of cellular turnover and requisite long-term self-renewal. Therefore, the DNA damage response and cell cycle regulation play a clear role in maintaining homeostasis without neoplastic progression. Here we will argue on the basis of recent advances in our understanding of tumor suppressor mechanisms in immune cells; however, that aspects of these same beneficial pathways have the potential to induce intrinsic immune aging.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725203 | PMC |
| http://dx.doi.org/10.1016/j.coi.2009.05.011 | DOI Listing |
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