Evidence map›Paper›PMID 41142312›Full record

ArticlePeerJ2025

Mendelian randomization and nomogram-based prediction of hepatocellular carcinoma risk in patients with hepatitis B cirrhosis.

Xiaolong Zheng, Yiping Hong, Wei Wei

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Xiaolong ZhengDepartment of Gastroenterology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Yiping HongDepartment of Gastroenterology, The Affiliated Jinhua Hospital, Zhejiang University School of Medicine, JinHua, China.
Wei WeiDepartment of Gastroenterology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Carcinoma, HepatocellularHepatitis BLiver CirrhosisLiver NeoplasmsMendelian Randomization AnalysisNomogramsAdultFemaleHumansLipoproteins, LDLMaleMiddle AgedRetrospective StudiesRisk AssessmentRisk FactorsLipoproteins, LDLClinical indicatorsHepatitis B-related cirrhosisHepatocellular carcinomaMendelian randomizationNomogram

Identifiers

PMID41142312
PMCPMC12548634

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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 OpenQuestion graph.