ArticleDiscover oncology2025
Mendelian randomization analysis of inflammatory biomarkers and hepatocellular carcinoma risk: genetic causality and single-cell transcriptomics.
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 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity.Current oncology reports · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundThe causal relationship between inflammatory biomarkers and hepatocellular carcinoma (HCC) risk remains unclear. This study aimed to investigate the causal associations between various inflammation-related biomarkers and HCC risk using Mendelian randomization (MR) analysis, complemented by single-cell transcriptomic validation.
methodsWe conducted comprehensive MR analyses using multiple statistical approaches including MR Egger, weighted median, inverse variance weighted, weighted mode, and simple mode methods to evaluate causal relationships between inflammatory biomarkers and HCC risk. Over 20-30 single nucleotide polymorphisms (SNPs) were employed as instrumental variables for each biomarker. Single-cell RNA sequencing data from four HCC samples (BT1306, BT1307, scrSOL004, scrSOL006) were analyzed to validate findings through cellular heterogeneity analysis, cell-cell communication networks, and pathway enrichment analysis.
resultsMR analysis identified differential causal effects of inflammatory biomarkers on HCC risk. Protective factors included CCL7 (OR: 0.524-0.714), CCL11 (OR: 0.660-0.752), IFN-gamma (OR: 0.657), NT-3 (OR: 0.520), and TWEAK_TNFSF12 (OR: 0.804), suggesting these factors may reduce HCC risk through immune modulation. Conversely, risk factors comprised CASP-8 (OR: 1.530), CD5 (OR: 2.079), FGF-21 (OR: 2.052), and CCL2 (OR: 2.440), with CCL2 showing the strongest pathogenic association. Single-cell analysis successfully identified 29 distinct cell subpopulations and revealed complex intercellular communication networks involving MIF, MK, and ncWNT signaling pathways. CCL2 and CCL8 demonstrated significant positive correlation (r = 0.4362, p < 0.001) across multiple cell types, with fibroblasts and malignant cells serving as central communication hubs.
conclusionsThis study provides robust genetic evidence for causal relationships between specific inflammatory biomarkers and HCC risk through MR analysis.
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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.