ReviewWorld journal of hepatology2022
Immunomodulation by probiotics and prebiotics in hepatocellular carcinoma.
Review in World journal of hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 16 citations in OpenAlex.
- The gut-liver-virus axis in hepatitis B and C: microbiota, immunometabolism, and exosome-mediated therapeutic opportunities.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Bibliometric Analysis of Gut Microbiota and Hepatocellular Carcinoma: Research Trends and Frontiers.Journal of hepatocellular carcinoma · 2026Article
- Gut Microbiota and Hepatocellular Carcinoma: Metabolic Products and Immunotherapy Modulation.Cancer medicine · 2025Review
- Gut Microbiota and the Gut-liver Axis in Hepatocellular Carcinoma: A Comprehensive Review of Pathogenesis and Therapeutic Strategies.Anti-cancer agents in medicinal chemistry · 2025Review
- Emerging insights into the gut microbiota as a key regulator of immunity and response to immunotherapy in hepatocellular carcinoma.Frontiers in immunology · 2025Review
- Impact of gut microbiota on metabolic dysfunction-associated steatohepatitis and hepatocellular carcinoma: pathways, diagnostic opportunities and therapeutic advances.European journal of medical research · 2024Review
- The Gut-Organ Axis within the Human Body: Gut Dysbiosis and the Role of Prebiotics.Life (Basel, Switzerland) · 2023Review
- Potential Effects of Regulating Intestinal Flora on Immunotherapy for Liver Cancer.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the most prevalent primary malignancy in patients suffering from chronic liver diseases and cirrhosis. Recent attention has been paid to the involvement of the gut-liver axis (GLA) in HCC pathogenesis. This axis results from a bidirectional, anatomical and functional relationship between the gastrointestinal system and the liver. Moreover, the complex network of interactions between the intestinal microbiome and the liver plays a crucial role in modulation of the HCC-tumor microenvironment, contributing to the pathogenesis of HCC by exposing the liver to pathogen-associated molecular patterns, such as bacterial lipopolysaccharides, DNA, peptidoglycans and flagellin. Indeed, the alteration of gut microflora may disturb the intestinal barrier, bringing several toll-like receptor ligands to the liver thus activating the inflammatory response. This review explores the new therapeutic opportunities that may arise from novel insights into the mechanisms by which microbiota immunomodulation, represented by probiotics, and prebiotics, affects HCC through the GLA.
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.