ArticleCanadian journal of gastroenterology & hepatology2026
Novel Potential Markers of Metabolic Dysfunction-Associated Steatohepatitis Prone to Hepatocellular Carcinoma.
Article in Canadian journal of gastroenterology & hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Novel Potential Markers of Metabolic Dysfunction-Associated Steatohepatitis Prone to Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundMetabolic dysfunction-associated steatohepatitis (MASH), the progressive phenotype of metabolic dysfunction-associated steatotic liver disease (MASLD), is well recognized for its increased risk of progressing to cirrhosis and hepatocellular carcinoma (HCC). However, early diagnosis and identification of the MASH patients with a tendency toward malignancy HCC remain a significant challenge.
methodIn previous studies, we established a novel conditional inducible HRAS gene expression murine model with normal diet and lifestyle conditions, which exhibited 100% HCC incidence and recapitulated the four major progression stages of MASH to HCC: MASH, fibrosis, cirrhosis, and HCC. Based on this model, we revealed the potential markers of MASH prone to HCC characteristics of malignant MASH through RNA-Seq and bioinformatics analysis, and further confirmed by pathological biopsy, biochemical tests, inflammatory cytokines measurement, Oil O red staining, and immunohistochemical examination.
resultsFor MASH, the initial stage of HCC, we observed evidence of hyperlipidemia and insulin resistance in the HRAS mouse model based on blood morphology, biochemical parameters, and insulin tolerance test. Furthermore, the pathological features of MASH were confirmed by the presence of hepatocellular fatty vacuolar changes, lipid droplet accumulation, and inflammation. Then, RNA-Seq analysis revealed the molecular signatures of malignant MASH and revealed three novel potential markers associated with adverse progression of MASH to HCC: Klk1b4, Alox5, and Pla2g2e.
conclusionBased on a stable and novel murine model of MASH prone to HCC, we, for the first time, presented a comprehensive molecular signature and identified novel potential adverse progression markers of MASH prone to malignant HCC, which contributed possibly to early clinical diagnosis and prognostic assessment, even becoming potential therapeutic target.
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.