Narrative review: therapy-induced senescence and cancer treatment resistance
This narrative review links therapy-induced senescence to cancer treatment resistance across chemotherapy, radiotherapy, targeted therapy and immunotherapy, but says current data do not establish it as a universal or independent cause of treatment failure. [1]
Automatic summary · not editorially reviewed
The key findings
Therapy-induced senescence may initially suppress tumor growth through durable proliferative arrest, while persistent senescent cells may in specific contexts contribute to recurrence or resistance. [1]
The review synthesizes mechanistic, translational and clinical evidence linking senescence to resistance across chemotherapy, radiotherapy, targeted therapy and immunotherapy. [1]
Current data support a context-dependent role for persistent senescence in treatment resistance but do not establish therapy-induced senescence as a universal or independent cause of therapeutic failure. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- Cancer treatment contexts described in the review, including chemotherapy, radiotherapy, targeted therapy and immunotherapy, and tissues that may contain pre-existing senescent populations.
- Summary based on
- Study abstract
- Original publication
- September 23, 2026
Senescence as a context-dependent stress response
The review describes cellular senescence as a heterogeneous stress response that depends on context and can influence how cancer responds to treatment. Therapy-induced senescence may first suppress tumor growth through lasting arrest of cell division. If senescent cells persist, they may in specific contexts contribute to recurrence or resistance, for example through signaling linked to the senescence-associated secretory phenotype (SASP), metabolic and epigenetic remodeling, cellular plasticity, immune evasion and changes in the tumor microenvironment.
Supporting source [1]
Evidence across four treatment types and biomarker limits
The authors synthesize mechanistic, translational and clinical evidence linking senescence to resistance across chemotherapy, radiotherapy, targeted therapy and immunotherapy. They explicitly separate experimental mechanisms, clinical associations and evidence that has or has not undergone prospective validation. Particular attention goes to SASP signaling, cellular plasticity and cancer stemness, senescence escape, metabolic adaptation, immune surveillance and biomarker limitations. They also evaluate emerging senolytic and senomorphic strategies and the sequential "one-two punch" paradigm, stressing differences between preclinical proof-of-concept and clinical evidence.
Supporting source [1]
Pre-existing senescent cells and translation barriers
The review notes that therapy-induced senescence also develops within tissues that may already contain senescent populations generated by aging, chronic inflammation, environmental stress, metabolic dysfunction, fibrosis or oncogenic signaling. Overall, the authors conclude that current data support a context-dependent role for persistent senescence in treatment resistance but do not establish therapy-induced senescence as a universal or independent cause of therapeutic failure. Clinical translation remains limited by senescence heterogeneity, lack of validated biomarkers, treatment toxicity, uncertainty about timing and insufficient prospective trials.
Supporting source [1]
How to interpret this
This is an abstract of a narrative review; the full text was not reviewed. The abstract reports no study design details, sample sizes, follow-up or prospective trial data, and the authors themselves note that clinical translation is limited by senescence heterogeneity, lack of validated biomarkers, treatment toxicity, uncertainty about timing and insufficient prospective trials.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Blanco JR, Carnero A. · europepmc.org · September 23, 2026