ArticleDiscover oncology2025
Mendelian randomization analysis of druggable gene expression in liver cancer risk and autoimmune hepatitis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLiver cancer remains one of the most prevalent and lethal malignancies worldwide, while autoimmune hepatitis is an immune-mediated inflammatory liver disease characterized by circulating autoantibodies and distinctive histopathological features. Mendelian Randomization (MR), as an innovative epidemiological research method, providing a reliable approach for exploring causal relationships between gene expression and liver disease risk.
methodsThis study employed a comprehensive two-sample Mendelian randomization analytical approach to systematically evaluate the causal relationships between druggable gene expression levels and liver disease risk, including both liver cancer and autoimmune hepatitis. The study incorporated expression quantitative trait loci (eQTL) data from 4,479 druggable genes as exposure variables, with liver cancer genome-wide association study (GWAS) data and autoimmune hepatitis GWAS data serving as outcome variables.
resultsMendelian randomization analysis revealed significantly different impacts of multiple gene expression levels on liver disease outcomes. For liver cancer, high expression of CCL7 and CCL11 genes demonstrated protective effects, with CCL11 gene showing statistical significance (HR = 0.600, 95%CI: 0.409-0.953, p = 0.027), suggesting these genes may exert protective functions through immune response regulation mechanisms. Conversely, high expression of CASP8, CD5, and FGF21 genes significantly increased patient mortality risk.
conclusionsThis study provides sufficient and reliable scientific evidence for liver disease risk-related genes through multidimensional Mendelian randomization validation analysis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.