Home Research Feeds Distinct alterations of gut microbiota between viral- and non-viral-related hepatocellular carcinoma

Distinct alterations of gut microbiota between viral- and non-viral-related hepatocellular carcinomaOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-05

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
Thailand
Sample Site
Feces
Species
Homo sapiens

What was studied?

This study compared gut microbiota between viral-related and non-viral hepatocellular carcinoma (HCC). It used 16S rRNA sequencing of the V3-V4 region on stool. The team also measured a fecal butyrate gene by qPCR and plasma markers of gut damage and microbial translocation. A random forest model built a diagnostic signature. The goal was to see whether cause of liver cancer leaves a distinct microbial fingerprint.

Who was studied?

The cohort was recruited in Bangkok, Thailand. It included 33 viral-HCC patients (17 hepatitis B, 16 hepatitis C) and 18 non-hepatitis B, non-hepatitis C HCC patients. Sixteen healthy adults served as controls, averaging 32.7 years. Non-viral patients were older than viral patients but similar in BMI, cirrhosis, and tumor stage. HIV-positive individuals were excluded, and antibiotics and probiotics were stopped before sampling.

What were the most important findings?

Non-viral HCC had lower alpha diversity than viral HCC (Simpson p = 0.013, Shannon p = 0.023). Sixteen genera separated the subgroups, with eleven reduced and five enriched in non-viral disease. Several short-chain fatty acid producers, including Faecalibacterium, were lower in non-viral cases. Fecal butyrate gene copies fell and plasma LBP rose in non-viral disease. The 16-genus random forest classifier reached an AUC of 0.94, with 97.0% sensitivity and 83.3% specificity.

What are the greatest implications of this study?

The results show gut dysbiosis differs by the cause of liver cancer, with non-viral disease marked by fewer short-chain fatty acid producers and more microbial translocation. A microbiota signature could help distinguish HCC subtypes noninvasively. The sample was small and single-center, and diet and environment were not fully captured. Findings are associations that need larger cohorts to confirm.

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