ArticleDiscover oncology2025
Inflammatory cytokines and oral cancer risk: an integrated study combining two-sample Mendelian randomization with experimental validation.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis 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.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
objectiveThis study aimed to investigate the causal relationship between inflammatory cytokines and oral cavity cancer risk using Mendelian randomization analysis and experimental validation.
methodsTwo-sample Mendelian randomization was conducted using summary-level genome-wide association study data on 41 inflammatory cytokines and oral cavity cancer risk in Europeans. Single nucleotide polymorphisms associated with cytokines (p < 5 × 10-6) and oral cancer were selected as instrumental variables, excluding those in linkage disequilibrium. Inverse-variance weighted analysis was used as the primary method, supplemented by MR Egger, weighted median, simple and weighted mode methods. Sensitivity analyses included heterogeneity, horizontal pleiotropy, leave-one-out, and funnel plot assessments. Multivariable MR analysis adjusted for smoking, alcohol, periodontitis and malnutrition was performed. The findings were further validated through expression analysis in TCGA database and clinical samples, as well as functional studies in oral cancer cells.
resultsIn univariate MR analysis, increased beta-nerve growth factor (OR: 1.53, 95% CI: 1.06-2.20), and decreased macrophage colony stimulating factor (OR: 0.87, 95% CI: 0.78-0.98) and interleukin-18 (OR: 0.80, 95% CI: 0.65-0.98) were causally associated with higher oral cancer risk. In multivariable MR analysis, the effects remained significant after adjusting for exposures. No reverse causation was found. Expression analysis revealed significant upregulation of NGF in oral cancer tissues compared to adjacent normal tissues, while CSF1 and IL-18 showed no significant differences. Functional studies demonstrated that NGF overexpression promoted cell proliferation, colony formation, invasion, and migration while inhibiting apoptosis in oral cancer cells.
conclusionsThis integrated study combining MR analysis and experimental validation provides evidence for causal effects of increased beta-nerve growth factor along with decreased macrophage colony stimulating factor and interleukin-18 on higher oral cavity cancer risk, independent of known risk factors. The oncogenic role of NGF was further confirmed through functional studies, suggesting these inflammatory cytokines may represent etiologic targets for oral cancer prevention.
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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 Socratic graph.