ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The CXCL10-CXCR3 Axis Induces Tumor-Associated Neutrophils to Interfere with CTLs-Mediated Antitumor Activity in EBV-Associated Epithelial Cancers.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Multifaceted roles of chemokines in gastric cancer: From tumor microenvironment modulation to therapeutic targeting (Review).Oncology letters · 2026Review
- Persistent NET states link lesion-related microbial signals to the cold tumor-related local restrictive environment: a context-dependent working model.Cell communication and signaling : CCS · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.Biomarker research · 2026Review
- miR-320d Is Associated with Reduced Nasopharyngeal Carcinoma Progression, Potentially through the NF-κB/IL-8 Axis-Mediated Inhibition of Neutrophil Extracellular Trap Formation.Oncology research · 2026Article
- Single-cell sequencing uncovers clonal dynamics profiles and therapeutic resistance biomarkers in relapsed and refractory peripheral T-cell lymphoma.Frontiers in immunology · 2026Article
- Neutrophils and neutrophil extracellular traps: double-edged swords in cancer pathophysiology and therapy resistance.Cell communication and signaling : CCS · 2025Review
- The CXCL10-CXCR3 Axis Induces Tumor-Associated Neutrophils to Interfere with CTLs-Mediated Antitumor Activity in EBV-Associated Epithelial Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
25 authors.
Funding
Abstract
Although Epstein-Barr virus (EBV)-associated epithelial cancers are categorized as immunologically "hot" tumors, they have unsatisfactory responses to immunotherapy. Increasing evidence has shown that therapeutic failure is due to an immunosuppressive tumor microenvironment established by EBV. In this study, a negative correlation is found between the infiltration of neutrophils and that of cytotoxic T lymphocytes (CTLs) containing granzyme B in EBV-associated epithelial cancers. The CXCL10-CXCR3 axis in EBV-associated epithelial cancer cells controls the extrusion of neutrophil extracellular traps (NETs), which interferes with the antitumor activity of EBV antigen-specific T cells in vitro and in vivo. NETs are positively correlated with the number of dysfunctional CTLs in EBV-associated epithelial cancers, and are confirmed to be an independent prognostic factor for patients with EBV-associated epithelial cancers. In conclusion, these findings reveal a novel mechanism of immunosuppression of tumor-associated neutrophils (TANs) in EBV-associated epithelial cancers. Targeting NETs formation in TANs may be a potential strategy for improving the efficacy of immunotherapy against EBV-associated epithelial cancers.
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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.