ArticleBMC cancer2025
CXCL8-dependent recruitment of neutrophils by the tumor microenvironment drives poor prognosis in glioblastoma patients.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The immunosuppressive tumor microenvironment in glioblastoma.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Glioblastoma remains a therapeutic challenge due to its immunosuppressive tumor microenvironment and resistance to immunotherapy. This study investigates the role of CXCL8 signaling in recruiting immunosuppressive neutrophils and driving poor prognosis in glioblastoma. Analysis of TCGA data revealed significant upregulation of CXCL8 in glioblastoma tissues, correlating with reduced survival and neutrophil chemotaxis pathway activation. We identified a distinct low-density neutrophil subpopulation (L-NEUs) in GBM patient blood, characterized by immature markers (CD16low, CD13low, CD10low) and CXCL8-dependent migration. Integrative bioinformatics identified RNASE2 and THBD as L-NEU-specific markers, both upregulated in GBM and associated with poor prognosis. Functional studies demonstrated that CXCL8 overexpression in macrophages enhanced L-NEU recruitment. RNASE2 (secretory) and THBD (transmembrane) emerged as dual biomarkers and therapeutic targets, with pan-cancer survival analysis linking their overexpression to adverse outcomes in glioblastoma, renal carcinoma, and others. These findings define CXCL8-driven neutrophil recruitment as a key immunosuppressive mechanism in glioblastoma and propose RNASE2/THBD-targeted strategies to improve immunotherapy efficacy.
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Registered trials
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