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Damaged cells can stop dividing permanently instead of dying. That protects against cancer at first, but senescent cells linger, secrete inflammatory signals, and after chemotherapy can help tumours relapse, so removing them (senolytics) is a new strategy.
Oncogene-induced and therapy-induced senescence engage p53/p21 and p16/RB to arrest the cycle; the senescence-associated secretory phenotype (SASP: IL-6, IL-8, MMPs) remodels the microenvironment, promotes inflammation, immune recruitment, and paradoxically tumour progression and treatment resistance. 'One-two punch' therapy induces senescence (e.g., CDK4/6 inhibitors, chemotherapy) then clears it with senolytics (BCL-XL/BCL-2 inhibitors, navitoclax; dasatinib+quercetin; uPAR CAR-T in mice). Senescent cells are a 2022 hallmark. Clinical proof in oncology is early; toxicity of BCL-XL inhibition (platelets) drives PROTAC approaches.
Retired workers who refuse to leave the office. They no longer do the job, but they shout, clutter the corridors, and sometimes hire back the very people who were fired.
Cancer is now understood to change its identity and behaviour without new mutations, to be shaped by bacteria inside and around it, and to be helped along by ageing cells. This explains why some tumours escape targeted drugs by changing cell type and why gut bacteria affect immunotherapy response.
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Shares Cold Spring Harbor Laboratory, Drug-tolerant persister cells and the tag mechanism.
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Shares Cold Spring Harbor Laboratory, CDK4/6 inhibitors, Memorial Sloan Kettering Cancer Center and the tag mechanism.