ArticleScience (New York, N.Y.)2018
Neutrophil extracellular traps produced during inflammation awaken dormant cancer cells in mice.
Article in Science (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 982 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.
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
982 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,389 citations in OpenAlex.
- From immunological mechanisms to targeted therapies: a bibliometric analysis in the domain of research concerning neutrophil extracellular traps and pulmonary diseases (2006-2025).Frontiers in immunology · 2026Pooled it
- Immune-inflammation index as prognostic markers in metastatic castration-resistant prostate cancer: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Novel lipid nanoparticle in a mRNA cancer vaccine drives tumor control via type I IFNs and effector CD8Molecular therapy. Nucleic acids · 2026Article
- Niches in cancer: from primary tumors to metastatic disease.Journal of hematology & oncology · 2026Review
- The immune phenotype of circulating tumor cells: from escape mechanisms to immunotherapy navigation.Biomarker research · 2026Review
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Systemic health impact of cancer-associated extracellular vesicles and particles.Nature reviews. Cancer · 2026Review
- Review
- A CTC/DTC-centered temporal framework of bone metastasis: From dissemination to dormancy and reactivation.Journal of bone oncology · 2026Review
- DVT-primed neutrophils reshape the brain microenvironment to promote brain metastasis.bioRxiv : the preprint server for biology · 2026Article
- PAD4-DB: A Curated Structure-Activity Resource Reveals Hub-Organized Activity Cliffs and Scaffold-Dependent SAR Ruggedness in PAD4 Inhibitors.International journal of molecular sciences · 2026Article
- Neutrophil Extracellular Traps in the Tumor Microenvironment: Mechanisms, Immune Regulation, and Implications for Immune Checkpoint Inhibitor Therapy.International journal of molecular sciences · 2026Review
- Article
- Leveraging Microphysiological Systems to Facilitate Neutrophil-Based Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- NNMT-associated metabolic-thromboinflammatory-immune co-activation in heterogeneous CTC clusters: a hypothesis-generating computational framework".BMC cancer · 2026Article
- Neutrophils in cancer.Nature reviews. Cancer · 2026Review
- Advancing the applications of liquid biopsies in oncology.Nature reviews. Genetics · 2026Review
- Does acute inflammation triggered by infection promote cancer progression?PLoS biology · 2026Review
- Pathway potency in methylation altered network reveals lung cancer branching evolution and hallmarks.iScience · 2026Article
- Article
922 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
Abstract
Cancer cells from a primary tumor can disseminate to other tissues, remaining dormant and clinically undetectable for many years. Little is known about the cues that cause these dormant cells to awaken, resume proliferating, and develop into metastases. Studying mouse models, we found that sustained lung inflammation caused by tobacco smoke exposure or nasal instillation of lipopolysaccharide converted disseminated, dormant cancer cells to aggressively growing metastases. Sustained inflammation induced the formation of neutrophil extracellular traps (NETs), and these were required for awakening dormant cancer. Mechanistic analysis revealed that two NET-associated proteases, neutrophil elastase and matrix metalloproteinase 9, sequentially cleaved laminin. The proteolytically remodeled laminin induced proliferation of dormant cancer cells by activating integrin α3β1 signaling. Antibodies against NET-remodeled laminin prevented awakening of dormant cells. Therapies aimed at preventing dormant cell awakening could potentially prolong the survival of cancer patients.
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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.