ArticleJournal of inflammation research2024
Exploring the Role of Inflammatory Genes and Immune Infiltration in Vestibular Schwannomas Pathogenesis.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Transcriptomic meta-analysis identifies dysregulated pathways and potential therapeutic targets in Vestibular Schwannoma.PloS one · 2026Pooled it
- Matrix Metalloproteinase‑9 (MMP-9) Activatable Gold Nanoparticles forACS applied nano materials · 2026Article
- Molecular and genetic insights into vestibular schwannoma.Journal of neuro-oncology · 2026Review
- Gallbladder Schwannoma: A Case Report and Literature Review.Diagnostics (Basel, Switzerland) · 2025Article
- Current molecular understanding of central nervous system schwannomas.Acta neuropathologica communications · 2025Review
- Integrative Bulk and Single-Cell Transcriptome Analyses Reveal Mitochondrial Metabolism-Related Biomarkers in IgA Nephropathy with Experimental Validation.Journal of inflammation research · 2025Article
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Authors and funding
6 authors.
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Abstract
Background: Vestibular schwannomas (VSs) exhibit a range of tumor behaviors, such as growth patterns and auditory dysfunction. Recent research has offered insights into the inflammatory microenvironment in modulating tumor dynamics. This study investigates the role of inflammatory genes and immune infiltration in VS pathogenesis. Methods: We retrieved mRNA microarray data of VSs and normal nerves from the GEO database (GSE141801, GSE108524, and GSE56597), focusing on bioinformatic analysis of inflammatory response genes. Based on the evidence provided by bioinformatics analysis, we assessed the expression levels of Iba-1, IL-10, IL-10RA, and IL-18 in 31 VS patients via immunohistochemistry and delved into their association with tumor size and auditory dysfunction. Results: We identified 1117 differentially expressed genes (DEGs) in VSs compared to normal nerves, showing an upregulation in inflammatory pathways. Intersection with inflammatory response genes (IRG) yielded 41 significant IRG-DEGs. Network analysis identified a core module of 10 IRG-DEGs and 11 hub genes, most of which were inflammatory cytokines. Immune infiltration analysis showed macrophage activation and M2 polarization. These findings were validated in an independent dataset (GSE39645). To further explore the association between inflammation and tumor behaviors, immunohistochemistry analysis was conducted on VS samples and the results exhibited notable associations between the macrophage marker (Iba1) and inflammatory cytokines (IL-10, IL-10RA, and IL-18) with both tumor size and auditory dysfunction. In particular, the multiple regression analysis of inflammatory cytokines demonstrated that IL-10 and IL-10RA were statistically significant predictors of tumor size, while IL-18 was associated with hearing loss. Conclusion: Our study underscores the role of inflammation in VS pathogenesis, showing that macrophage activation with M2 polarization and the expression of inflammatory cytokines, especially IL-10/IL-10RA and IL-18, are linked to tumor size and auditory function. This study highlights the inflammatory landscape's impact on VS behaviors, providing a basis for targeted therapeutic strategies.
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