ArticleFrontiers in immunology2023
Bladder cancer patients have increased NETosis and impaired DNaseI-mediated NET degradation that can be therapeutically restored
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Delving into the clinical impact of NETs in pediatric cancer.Pediatric research · 2025Pooled it
- Pediatric patients with cancer exhibit increased neutrophil extracellular traps and reduced active deoxyribonuclease I: diagnostic, prognostic, and therapeutic opportunities.Clinical and experimental pediatrics · 2026Article
- Neural regulation in lung cancer: from mechanisms to new therapeutic perspectives.Clinical and experimental medicine · 2026Review
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- Regulated cell death-induced coagulation dysfunction in sepsis.Journal of thrombosis and thrombolysis · 2026Review
- A comprehensive plasma-based approach to thromboinflammation in bladder cancer: integrating lipidomics, thrombin generation, and NETosis biomarkers.Journal of translational medicine · 2026Article
- Review
- The hypoxic ECM and neutrophils in MIBC immunotherapy resistance.Nature reviews. Urology · 2026Review
- Research progress on neutrophil extracellular traps and hepatitis-to-hepatocellular carcinoma transformation (Review).Oncology letters · 2026Review
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- Neutrophil extracellular traps in tumor metastasis: mechanisms, and therapeutic implications.Discover oncology · 2025Review
- Interplay between NETosis and the lncRNA-microRNA regulatory axis in the immunopathogenesis of cancer.Journal of physiology and biochemistry · 2025Review
- Neutrophil extracellular traps in cancer: From mechanisms to treatments.Clinical and translational medicine · 2025Review
- Pulmozyme Ameliorates LPS-Induced Lung Fibrosis but Provokes Residual Inflammation by Modulating Cell-Free DNA Composition and Controlling Neutrophil Phenotype.Biomolecules · 2025Article
- NETs - as predictors and targets of supportive therapy for cancer treatment.Frontiers in immunology · 2025Review
- Mechanistic roles of neutrophil heterogeneity in tumour pathogenesis.Frontiers in immunology · 2025Review
- Article
- Neutrophil Extracellular Traps and Endometriosis: Insights from a Case-Control Study.International journal of women's health · 2025Article
- Neutrophil extracellular traps and cannabinoids: potential in cancer metastasis.Frontiers in oncology · 2025Review
- Key immune cells and their crosstalk in the tumor microenvironment of bladder cancer: insights for innovative therapies.Exploration of targeted anti-tumor therapy · 2025Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Neutrophils, key players of the immune system, also promote tumor development through the formation of neutrophil extracellular traps (NETs) in a process called NETosis. NETs are extracellular networks of DNA, histones and cytoplasmic and granular proteins (calprotectin, myeloperoxidase, elastase, etc.) released by neutrophils upon activation. NETs regulate tumor growth while promoting angiogenesis and invasiveness, and tumor cells also stimulate NETosis. Although NETosis seems to be increased in cancer patients, an increase of NETs in plasma may also be mediated by an impaired degradation by plasma DNaseI, as evidenced in several immunological disorders like lupus nephritis. However, this has never been evidenced in bladder cancer (BC) patients. Herein, we aimed to evaluate the occurrence of increased NETosis in plasma and tumor tissue of BC patients, to ascertain whether it is mediated by a reduced DNaseI activity and degradation, and to Methods: We recruited 71 BC patients from whom we obtained a plasma sample before surgery and a formalin-fixed paraffin embedded tumor tissue sample, and 64 age- and sex-matched healthy controls from whom we obtained a plasma sample. We measured NETs markers (cell-free fDNA, calprotectin, nucleosomes and neutrophil elastase) and the DNaseI activity in plasma with specific assays. We also measured NETs markers in BC tissue by immunofluorescence. Finally, we evaluated the ability of BC and control plasma to degrade Results: NETosis occurs in BC tissue, more profusely in the muscle-invasive subtype ( Conclusion: To the best of our knowledge, this is the first report demonstrating that BC patients have an increased NETosis systemically and in the tumor microenvironment, in part caused by an impaired DNaseI-mediated NET degradation. Remarkably, this defect can be therapeutically restored
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