ArticlePeerJ2025
Mendelian randomization and nomogram-based prediction of hepatocellular carcinoma risk in patients with hepatitis B cirrhosis.
Article in PeerJ, 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.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: To innovatively integrate genetic causality and multidimensional clinical indicators, we aimed to investigate causal relationships between metabolic-inflammatory biomarkers and hepatocellular carcinoma (HCC) risk in hepatitis B-related cirrhosis (HBV-C) using Mendelian randomization (MR), and develop a precision prediction model combining genetic evidence with nonlinear biochemical dynamics. Methods: Leveraging bidirectional approaches, we first performed two-sample MR analysis on GWAS datasets (UK Biobank, Results: MR analysis revealed a robust causal link between reduced LDL levels and elevated HCC risk (OR = 0.472, 95% CI [0.259-0.860]; Conclusion: This study introduces a novel causal inference-guided prediction model, addressing the long-standing debate on LDL's dual role in hepatocarcinogenesis. By integrating MR-validated genetic causality, nonlinear biochemical modeling, and PCA-driven dimensionality reduction, our model provides a transformative tool for personalized HCC risk stratification in HBV-C patients.
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