Precancerous condition | Identified senescence-associated markers | Reference |
---|---|---|
Actinic keratosis | γH2AX | Hida et al., 2009 |
Bowen’s disease | p27Kip1 | Oh and Penneys, 2004 |
Ductal carcinoma in situ | p53, DEC1, and DCR2 | Pare et al., 2019 |
Lichen planus | p21Cip1 | Bascones-Ilundain et al., 2007 |
Oral leukoplakia | Rb | Bascones-Martínez et al., 2012 |
Colonic adenomas | p16INK4a | Kriegl et al., 2011 |
Cervical intraepithelial neoplasia | p15INK4b, p16INK4a, and p21Cip1 | Zhang et al., 2014 |
This table summarizes examples of experimental evidence demonstrating the expression of senescence-associated biomarkers in human tissue specimens derived from premalignant lesions. Increased expression of SA-β-gal is the canonical marker of the senescent phenotype. Rb, p15INK4b, p16INK4a, p21Kip1, and p21Cip1 are cell cycle regulators that are often involved in the initiation or maintenance of the senescent growth arrest. p53 is an established player in mediating DNA damage–induced senescence, whereas the phosphorylated form of H2A histone family member X (γH2AX) is a histone modification that reflects the development of DNA double-stranded breaks that often accompany senescence induction. Deleted in esophageal cancer 1 (DEC1) is a basic helix-loop-helix transcription factor that is involved in p53-mediated senescence, and decoy receptor 2 (DCR2) is a novel marker of senescence especially of the renal epithelium. None of these markers is specific to senescence, but all are frequently utilized in the experimental identification of senescence.