Correction: Biological aging marker p16^INK4a in T cells and breast cancer risk (Cancers 2020, 12, 3122)

The authors wish to make the following corrections to this paper [1]: An incorrect draft version was inadvertently submitted to the journal. The corrected version is now provided. The first two paragraphs in the Introduction section should be revised to: Elevated production of stress hormones due to stress exposure can increase DNA damage [1,2]. Excessive DNA damage can initiate cellular senescence and further accelerate biological aging [3]. The cell cycle inhibitor p16INK4a is a well-known biomarker for cellular senescence. The expression of p16INK4a due to stress exposure and DNA damage can prevent the replication of cells with severe DNA damage [4]. However, persistent cellular senescence via heightened p16INK4a can become detrimental because certain senescent cells may release pro-inflammatory factors to promote inflammation, damage nearby cells and tissues, further accelerate biological aging, and consequently increase the risk of age-related diseases [3,5]. Intriguingly, studies in mice have shown that eliminating p16INK4a-positive cells not only reduced cellular aging but also hindered tumor growth and reduced tumor progression [6]. This suggests that senescent cells play an essential role in age-related deterioration and tumorigenesis. Furthermore, the expression of p16INK4a is not an epiphenomenon of aging but appears to play a causal role in the age-associated replicative decline of several tissues, including T-cells [7]. The updated references in this paragraph are as below: 1. Flint, M.S.; Baum, A.; Chambers, W.H.; Jenkins, F.J. Induction of DNA damage, alteration of DNA repair and transcriptional activation by stress hormones. Psychoneuroendocrinology 2007, 32, 470–479. Epub 27 April 2007. doi: 10.1016/j.psyneuen.2007.02.013. 2. Hara, M.R.; Kovacs, J.J.; Whalen, E.J.; Rajagopal, S.; Strachan, R.T.; Grant, W.; Towers, A.J.; Williams, B.; Lam, C.M.; Xiao, K.; et al. A stress response pathway regulates DNA damage through beta2-adrenoreceptors and beta-arrestin-1. Nature 2011, 477, 349–353. doi: 10.1038/nature10368. 3. Campisi, J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell 2005, 120, 513–522. doi: 10.1016/j.cell.2005.02.003. 4. Campisi, J.; d’Adda, di Fagagna F. Cellular senescence: When bad things happen to good cells. Nat. Rev. Mol. Cell Biol. 2007, 8, 729–740. doi: 10.1038/nrm2233. 5. Coppe, J.P.; Desprez, P.Y.; Krtolica, A.; Campisi, J. The senescence-associated secretory phenotype: The dark side of tumor suppression. Annu. Rev. Pathol. 2010, 5, 99–118. doi: 10.1146/annurev-pathol-121808-102144.