What this means
This review looks at how cells that stop dividing after cancer treatment might sometimes help tumors survive. The authors say these cells play a role only in some cases, not in every case.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A narrative review of mechanistic, clinical, and lab evidence
- Kind of research
- A summary of earlier studies
The science
- Original title
- Therapy-Induced Senescence in Cancer Treatment Resistance: Mechanisms, Evidence, and Translational Opportunities.
- Authors
- Blanco JR, Carnero A
- Journal
- Cancers
- Published
- Oct 16, 2026
- Study type
- Review
- PMID
- 42882779 ↗
Abstract
Cellular senescence is a heterogeneous and context-dependent stress response that can influence cancer treatment response. Therapy-induced senescence (TIS) may initially suppress tumor growth through durable proliferative arrest, whereas persistence of senescent cells may, in specific contexts, contribute to recurrence or resistance through SASP-mediated signaling, metabolic and epigenetic remodeling, cellular plasticity, immune evasion, and changes in the tumor microenvironment. TIS also develops within tissues that may contain pre-existing senescent populations generated by aging, chronic inflammation, environmental stress, metabolic dysfunction, fibrosis, or oncogenic signaling. In this narrative review, we synthesize mechanistic, translational, and clinical evidence linking senescence to resistance across chemotherapy, radiotherapy, targeted therapy, and immunotherapy. We explicitly distinguish experimental mechanisms, clinical associations, and evidence that has or has not undergone prospective validation. Particular attention is given to SASP signaling, cellular plasticity and cancer stemness, senescence escape, metabolic adaptation, immune surveillance, and biomarker limitations. We further evaluate emerging senolytic and senomorphic strategies and the sequential "one-two punch" paradigm, emphasizing differences between preclinical proof-of-concept and clinical evidence. Overall, current data support a context-dependent role for persistent senescence in treatment resistance, but do not establish TIS as a universal or independent cause of therapeutic failure. Clinical translation remains limited by senescence heterogeneity, lack of validated biomarkers, treatment toxicity, uncertainty regarding timing, and insufficient prospective trials.
Blanco JR, Carnero A Therapy-Induced Senescence in Cancer Treatment Resistance: Mechanisms, Evidence, and Translational Opportunities. Cancers. 2026. doi:10.3390/cancers18193084. PMID: 42882779. https://pubmed.ncbi.nlm.nih.gov/42882779/
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