What this means
This review looks at how cancer treatments can leave cells in a state of stress called senescence. It explains how these cells may help or hurt the immune system.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of earlier research, with no new experiments
- Kind of research
- A summary of earlier studies
The science
- Original title
- Reshaping the tumor immune microenvironment via therapy-induced senescence: senescence-associated secretory phenotype networks and senolytic strategies.
- Authors
- Geng X, Li P, Xu K et al.
- Journal
- Molecular biology reports
- Published
- Oct 25, 2026
- Study type
- Review · in humans
- PMID
- 42927531 ↗
Abstract
Anticancer therapy can suppress tumor growth by inducing cell death, but many treatments also impose durable stress programs in malignant and stromal cells. Therapy-induced senescence (TIS) has emerged as a central non-lethal outcome of chemotherapy, radiotherapy and targeted therapy. Senescent cells remain metabolically active and communicate with their surroundings through the senescence-associated secretory phenotype (SASP), a heterogeneous mixture of cytokines, chemokines, growth factors, proteases, extracellular vesicles and immune-modulatory signals. In cancer, this secretory program can support immune surveillance when it is transient and efficiently cleared, yet it can also promote chronic inflammation, immune suppression, stromal remodeling, recurrence and resistance when senescent cells persist. This review summarizes the TIS-SASP-tumor immune microenvironment (TIME) axis, with emphasis on the molecular regulation of SASP, immune-cell-specific remodeling, the biphasic nature of SASP-mediated immunity and the rationale for sequential senogenic-senolytic therapy. Here, "senogenic" refers to interventions that induce cellular senescence, "senolytic" to approaches that selectively eliminate senescent cells, and "senomorphic" to strategies that suppress or remodel harmful senescence-associated phenotypes without necessarily killing senescent cells. We discuss how senolytics, senomorphics and immune checkpoint combinations may convert therapy-induced senescence from a liability into a therapeutically exploitable state. We also highlight the translational barriers that currently limit this strategy, including biomarker specificity, cell-type heterogeneity, treatment timing, safety and the need for spatially resolved monitoring of senescent niches.
Geng X, Li P, Xu K et al. Reshaping the tumor immune microenvironment via therapy-induced senescence: senescence-associated secretory phenotype networks and senolytic strategies. Molecular biology reports. 2026. doi:10.1007/s11033-026-13049-2. PMID: 42927531. https://pubmed.ncbi.nlm.nih.gov/42927531/
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