ArticleiLIVER2025
Detection of metabolic signatures implicated in the progression from hepatitis to cirrhosis to hepatocellular carcinoma.
Article in iLIVER, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- NUPR1 as a central stress-adaptation node in cancer: integrating metabolic rewiring, cell death, and therapy resistance.Journal of biomedical science · 2026Review
- Metabolic dynamics and stage-specific biomarkers in chronic HBV infection: a metabolomics study.BMC gastroenterology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and aims: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. The mechanisms driving the transition from hepatitis to cirrhosis, and eventually, to HCC are unclear. This study aimed to clarify the metabolic changes that underly the progression of HCC and identify potential prognostic and therapeutic biomarkers. Methods: This prospective study collected serum samples from patients with chronic hepatitis, cirrhosis, or HCC, hospitalized at the Fifth Medical Center of the PLA General Hospital, from December 2022 to December 2023. The samples were analyzed using non-targeted, ultra-high-performance liquid chromatography and mass spectrometry. Partial least squares-discriminant analysis modeling and Results: We identified 153 differentially expressed metabolites in the progression from hepatitis to cirrhosis to HCC, many of which were involved in ammonia cycling or the metabolism of methylhistidine, alanine, arginine, proline, or betaine. We also identified L-histidine and adenosine as the metabolites that demonstrated significant sensitivity and specificity for distinguishing among the hepatitis, cirrhosis, and HCC stages. Conclusions: Our study comprehensively characterized the metabolic profiles of the different stages of the hepatitis-cirrhosis-HCC transition. We showed that serum metabolite detection is a viable diagnostic tool for identifying and monitoring high-risk individuals, which could potentially be used to halt the development of HCC.
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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 Socratic graph.