ArticleInternational journal of experimental pathology2017
Hepatocellular carcinoma in a mouse model fed a choline-deficient, L-amino acid-defined, high-fat diet.
Article in International journal of experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 93 citations in OpenAlex.
- Blood Focused-Metabolomics and Transcriptomics Uncover Non-Linear Risk Association of Inadequate Dietary Choline Intake-Linked Metabolic Stress with MASLD Through Amino Acid Biomarkers,International journal of molecular sciences · 2026Article
- Comparison and Characteristics of MASLD Mouse Models.Biomedicines · 2026Review
- Susceptibility and transcriptional characteristics of inbred C57BL/6J and outbred ICR mice in CDAHFD-induced MASH models.Laboratory animal research · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Choline supplementation in classic homocystinuria: impact on homocysteine and hepatic steatosis.Pediatric research · 2026Article
- ModulatingJournal for immunotherapy of cancer · 2026Article
- Retatrutide improves steatohepatitis in an accelerated mouse model of diet-induced steatohepatitis with a fructose binge.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Endoplasmic reticulum stress at the forefront of fatty liver diseases and cancer.Pharmacological reviews · 2025Review
- [Pathology of liver tumours in animal models].Pathologie (Heidelberg, Germany) · 2025Review
- Beyond obesity: lean metabolic dysfunction-associated steatohepatitis from unveiling molecular pathogenesis to therapeutic advancement.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Evaluation of Serum L-FABP as a Biomarker and Hepatoprotective Effect of L-FABP Using Wild-Type and Human L-FABP Chromosome Transgenic Mice.Journal of the American Association for Laboratory Animal Science : JAALAS · 2025Article
- Review
- MASH as an emerging cause of hepatocellular carcinoma: current knowledge and future perspectives.Molecular oncology · 2025Review
- Current Treatment Regimens and Promising Molecular Therapies for Chronic Hepatobiliary Diseases.Biomolecules · 2025Review
- Article
- Establishment and characterization of mouse metabolic dysfunction-associated steatohepatitis-related hepatocellular carcinoma organoids.Scientific reports · 2024Article
- Article
- Galectin 3-binding protein (LGALS3BP) depletion attenuates hepatic fibrosis by reducing transforming growth factor-β1 (TGF-β1) availability and inhibits hepatocarcinogenesis.Cancer communications (London, England) · 2024Article
- Elevated choline drives KLF5-dominated transcriptional reprogramming to facilitate liver cancer progression.Oncogene · 2024Article
- Ginger essential oil prevents NASH progression by blocking the NLRP3 inflammasome and remodeling the gut microbiota-LPS-TLR4 pathway in mice.Nutrition & diabetes · 2024Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a common cancer worldwide and represents the outcome of the natural history of chronic liver disease. The growing rates of HCC may be partially attributable to increased numbers of people with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). However, details of the liver-specific molecular mechanisms responsible for the NAFLD-NASH-HCC progression remain unclear, and mouse models that can be used to explore the exact factors that influence the progression of NAFLD/NASH to the more chronic stages of liver disease and subsequent HCC are not yet fully established. We have previously reported a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) as a dietary NASH model with rapidly progressive liver fibrosis in mice. The current study in C57BL/6J mice fed CDAHFD provided evidence for the chronic persistence of advanced hepatic fibrosis in NASH and disease progression towards HCC in a period of 36 weeks. When mice fed CDAHFD were switched back to a standard diet, hepatic steatosis was normalized and NAFLD activity score improved, but HCC incidence increased and the phenotype of fibrosis-associated HCC development was observed. Moreover, when mice continued to be fed CDAHFD for 60 weeks, HCC further developed without severe body weight loss or carcinogenesis in other organs. The autochthonous tumours showed a variety of histological features and architectural patterns including trabecular, pseudoglandular and solid growth. The CDAHFD mouse model might be a useful tool for studying the development of HCC from NAFLD/NASH, and potentially useful for better understanding pathological changes during hepatocarcinogenesis.
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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.