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. 2022 Aug 3;18(10):611–627. doi: 10.1038/s41581-022-00601-z

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Fig. 2 — Most carcinogenic mutations induce senescence through the p53–p21 and p16–RB pathways, although some mutations activate p21 directly. Reactive oxygen species (ROS)-induced senescence in cancer cells is mainly dependent on p16, p21 and/or p27. Senescence-induced cell-cycle arrest can prevent mutations from being passed on to the next generation of cells and accelerate immune clearance, resulting in suppression of tumurigenesis. However, the senescence-associated secretory phenotype (SASP) also contributes to a pro-inflammatory and growth-stimulatory microenvironment that can promote tumour development.