Correction: Shen, J.; et al. Biological Aging Marker p16INK4a in T Cells and Breast Cancer Risk. Cancers 2020, 12, 3122

The authors wish to make the following corrections to this paper [...].

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:  The fifth paragraph in the Discussion section should be revised to: The higher levels of p16INK4a mRNA expression in both cases and controls with a family history of cancer than those without are intriguing. Learning that a family member has cancer is a stressful event because it may unavoidably lead to the speculation about whether they will also have cancer due to their shared genetic background [29,30]. Previous studies in breast cancer have shown that women with a family history of breast cancer have higher levels of cancer-specific distress than those without a family history [31,32]. A positive coping style can encourage good psychological adjustment and thereby alleviate the stress. On the other hand, a negative coping style can further exacerbate stress and consequently lead to harmful health impacts [33,34]. Unfortunately, the current study did not collect data on coping styles.
The first three sentences of the sixth paragraph in the Discussion section should be revised to: The relationship between higher p16INK4a mRNA expression and breast cancer risk is expected. As mentioned previously, the expression of p16INK4a is a protective mechanism to guard against excessive DNA damage and prevent damaged cells from proliferating and causing further transformation to malignancy [3,4]. However, persistently elevated p16INK4a mRNA expression may have a detrimental consequence. Specific senescent cells may secrete pro-inflammatory cytokines, growth factors, and matrix-remolding enzymes that can cause damage to nearby cells or tissues and further promote tumorigenesis [5,35].
Since the number of cited references in the first two paragraphs are changed from 17 to 7, and one within the 17 but not the 7 is cited elsewhere in the paper, the total reference number is thus changed from 47 to 38. Therefore, the remaining reference numbers have been updated to 8-38.
The authors apologize for any inconvenience caused and state that the scientific conclusions are unaffected. The original article has been updated.

Conflicts of Interest:
The authors declare no conflict of interest.