ArticleJCI insight2019
Targetable mechanisms driving immunoevasion of persistent senescent cells link chemotherapy-resistant cancer to aging.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
108 citing papers in PubMed, 151 citations in OpenAlex.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Review
- Beyond bystanders: How β cell stress shapes the autoimmune response in T1D.Science translational medicine · 2026Review
- The Role of Cellular Senescence in Oral Health and Disease.International journal of molecular sciences · 2026Review
- NKGD2 Ligands (NKG2DLs) in Breast Cancer: In Silico Analysis and Narrative Review.International journal of molecular sciences · 2026Review
- The Immunogenicity of Human Senescent Cells Is Dependent on the Senescence Inducer and Cell Type.Aging cell · 2026Article
- Crosstalk between TGF-β and Wnt/β-catenin signaling drives fibrogenic and stem-like phenotypes in senescent MDA-MB-231 breast cancer cells.npj aging · 2026Article
- Review
- Differential responses to the combination of navitoclax and venetoclax with doxorubicin in murine models of triple negative breast cancer.Frontiers in cell and developmental biology · 2026Article
- Cellular senescence in cancer immunology and potential therapeutic strategy.Frontiers in oncology · 2026Review
- Tumor immunosenescence drives breast cancer progression and therapeutic resistance: mechanisms and emerging interventions.Frontiers in oncology · 2026Review
- Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.Frontiers in aging · 2026Review
- Tissue turnover and rejuvenation through mechanics.Frontiers in cell and developmental biology · 2026Review
- Senescent CD8 T Effector Memory Cells are Functionally Impaired, Enriched in Aging and Disease, and a Barrier to Immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- Targeting immunosenesence promotes clearance of senescent cells.Immunity & ageing : I & A · 2025Review
- Targeting Senescence in Oncology: An Emerging Therapeutic Avenue for Cancer.Current oncology (Toronto, Ont.) · 2025Review
- Cellular senescence offers distinct immunological vulnerabilities in cancer.Trends in cancer · 2025Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 1 country.
Funding
Abstract
Cellular senescence is a tumor suppressive mechanism that can paradoxically contribute to aging pathologies. Despite evidence of immune clearance in mouse models, it is not known how senescent cells (SnCs) persist and accumulate with age or in tumors in individuals. Here, we identify cooperative mechanisms that orchestrate the immunoevasion and persistence of normal and cancer human SnCs through extracellular targeting of natural killer receptor signaling. Damaged SnCs avoid immune recognition through MMPs-dependent shedding of NKG2D-ligands reinforced via paracrine suppression of NKG2D receptor-mediated immunosurveillance. These coordinated immunoediting processes are evident in residual, drug-resistant tumors from cohorts of >700 prostate and breast cancer patients treated with senescence-inducing genotoxic chemotherapies. Unlike in mice, these reversible senescence-subversion mechanisms are independent of p53/p16 and exacerbated in oncogenic RAS-induced senescence. Critically, the p16INK4A tumor suppressor can disengage the senescence growth arrest from the damage-associated immune senescence program, which is manifest in benign nevi lesions where indolent SnCs accumulate over time and preserve a non-pro-inflammatory tissue microenvironment maintaining NKG2D-mediated immunosurveillance. Our study shows how subpopulations of SnCs elude immunosurveillance, and reveals secretome-targeted therapeutic strategies to selectively eliminate -and restore the clearance of- the detrimental SnCs that actively persist after chemotherapy and accumulate at sites of aging pathologies.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.