ArticleNature2014
Tumour-infiltrating Gr-1+ myeloid cells antagonize senescence in cancer.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 2 of them syntheses that pooled it.
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.
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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.
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Who cites it
234 citing papers in PubMed, 2 syntheses or guidelines pooled it, 369 citations in OpenAlex.
- Pooled it
- A bibliometric and visual analysis of the impact of senescence on tumor immunotherapy.Frontiers in immunology · 2025Pooled it
- Prognostic Value of the Systemic Immune-Inflammation Index (SII) After Neoadjuvant Therapy for Patients with Resected Pancreatic Cancer.Annals of surgical oncology · 2020Trial
- Neutrophils in cancer.Nature reviews. Cancer · 2026Review
- Commensal Nakaseomyces glabratus migrates into prostate tumors to accelerate cancer progression.Nature cancer · 2026Article
- Therapy induced senescence promotes immunogenicity in acute myeloid Leukemia through reduced EZH2 activity.Nature communications · 2026Article
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- Oncogene inactivation-induced senescence facilitates tumor relapse.Nature communications · 2026Article
- The lethal symbiont: exploring the pathophysiology of cancer.Physiological reviews · 2026Review
- Tumor-derived CCL20 activates tumor-associated neutrophils, predicting good prognosis in endometrial cancer.Translational cancer research · 2026Article
- Immunological consequences of senescence in physiology and pathology.Journal of translational medicine · 2026Review
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- FOXA1 loss drives basal/squamous de-differentiation of prostate cancer and induces an immunosuppressive tumor microenvironment.Nature communications · 2026Article
- Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer.Molecular oncology · 2026Review
- Challenges and advances in drug resistance and tolerance in cancer.Journal of experimental & clinical cancer research : CR · 2026Review
- Integration of bulk and single-cell transcriptomic sequencing reveals the neutrophil heterogeneity in bladder cancer and establishes a prognostic model.Discover oncology · 2026Article
- A machine learning-defined cellular senescence signature systematically enhances prognostication and guides immunotherapy strategies for the treatment of gliomas.NPJ precision oncology · 2026Article
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- The molecular underpinnings of the immune landscape in prostate cancer: decoding a "cold" tumor.Frontiers in oncology · 2026Review
- From immune desert to hot tumor: the tripartite synergy of tumor microenvironment-exosomes-immunogenic cell death in pioneering solutions.Frontiers in immunology · 2026Review
174 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of oncogenes or loss of tumour suppressor genes opposes malignant transformation by triggering a stable arrest in cell growth, which is termed cellular senescence. This process is finely tuned by both cell-autonomous and non-cell-autonomous mechanisms that regulate the entry of tumour cells to senescence. Whether tumour-infiltrating immune cells can oppose senescence is unknown. Here we show that at the onset of senescence, PTEN null prostate tumours in mice are massively infiltrated by a population of CD11b(+)Gr-1(+) myeloid cells that protect a fraction of proliferating tumour cells from senescence, thus sustaining tumour growth. Mechanistically, we found that Gr-1(+) cells antagonize senescence in a paracrine manner by interfering with the senescence-associated secretory phenotype of the tumour through the secretion of interleukin-1 receptor antagonist (IL-1RA). Strikingly, Pten-loss-induced cellular senescence was enhanced in vivo when Il1ra knockout myeloid cells were adoptively transferred to PTEN null mice. Therapeutically, docetaxel-induced senescence and efficacy were higher in PTEN null tumours when the percentage of tumour-infiltrating CD11b(+)Gr-1(+) myeloid cells was reduced using an antagonist of CXC chemokine receptor 2 (CXCR2). Taken together, our findings identify a novel non-cell-autonomous network, established by innate immunity, that controls senescence evasion and chemoresistance. Targeting this network provides novel opportunities for cancer therapy.
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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.