Cellular senescence is a state of essentially irreversible cell-cycle arrest in which a cell stops dividing but remains alive, metabolically active, and comparatively resistant to apoptosis. It is marked by raised expression of cell-cycle inhibitors such as p16 and p21, by senescence-associated beta-galactosidase activity, and by a distinctive secretory program, the senescence-associated secretory phenotype.
Senescence can be triggered by replicative exhaustion, oncogene activation, or cytotoxic stress, so cancer therapy itself can drive tumor cells into a senescent rather than a dead state. Because senescent cells persist and keep secreting, they remain an influential, non-dividing component of a treated tumor. Senescent tumor cells are difficult to isolate from tissue, since no single reliable surface marker for them is yet available.
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Source papers
- Chemotherapy-induced senescence promotes stroma stiffness and antioxidant adaptation to promote chemoresistance in pancreatic ductal adenocarcinoma doi:10.1038/s41467-026-75772-5