ArticleJapanese journal of cancer research : Gann2002
Development of hepatocellular adenomas and carcinomas associated with fibrosis in C57BL/6J male mice given a choline-deficient, L-amino acid-defined diet.
Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 99 citations in OpenAlex.
- Myeloperoxidase, extracellular DNA and neutrophil extracellular trap formation in the animal models of metabolic dysfunction-associated steatotic liver disease.World journal of gastroenterology · 2025Article
- Progress in the Study of Animal Models of Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2024Review
- A Mouse Model of Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma Induced by Western Diet and Carbon Tetrachloride.Methods in molecular biology (Clifton, N.J.) · 2024Article
- New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023Review
- The bidirectional immune crosstalk in metabolic dysfunction-associated steatotic liver disease.Cell metabolism · 2023Review
- Establishment of Novel Mouse Model of Dietary NASH Rapidly Progressing into Liver Cirrhosis and Tumors.Cancers · 2023Article
- In Vivo and In Vitro Models to Study Liver Fibrosis: Mechanisms and Limitations.Cellular and molecular gastroenterology and hepatology · 2023Review
- An update on animal models of liver fibrosis.Frontiers in medicine · 2023Review
- Article
- Obesity, non-alcoholic fatty liver disease and hepatocellular carcinoma: current status and therapeutic targets.Frontiers in endocrinology · 2023Review
- Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research.International journal of molecular sciences · 2022Review
- Mouse models of nonalcoholic steatohepatitis and their application to new drug development.Archives of pharmacal research · 2022Review
- Article
- Nonobese mice with nonalcoholic steatohepatitis fed on a choline-deficient, l-amino acid-defined, high-fat diet exhibit alterations in signaling pathways.FEBS open bio · 2021Article
- Stress kinases in the development of liver steatosis and hepatocellular carcinoma.Molecular metabolism · 2021Review
- Analysis of differential neonatal lethality in cystathionine β-synthase deficient mouse models using metabolic profiling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- From Liver Fat to Cancer: Perils of the Western Diet.Cancers · 2021Review
- A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet.Lipids in health and disease · 2020Article
- Mouse Models of Oncoimmunology in Hepatocellular Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Review
- Targeted Nutrient Modifications in Purified Diets Differentially Affect Nonalcoholic Fatty Liver Disease and Metabolic Disease Development in Rodent Models.Current developments in nutrition · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Development of hepatocellular carcinomas in rats caused by a choline-deficient, L-amino acid-defined (CDAA) diet, usually associated with fatty liver, fibrosis, cirrhosis and oxidative DNA damage, has been recognized as a useful model of hepatocarcinogenesis caused by endogenous factors. In the present study, in order to further explore involved factors and genes, we established an equivalent model in spontaneous liver tumor-resistant C57BL/6J mice. Six-week-old males and females were continuously fed the CDAA diet and histological liver lesions and oxidative DNA damage due to 8-hydroxydeoxyguanosine (8-OHdG) were examined after 22, 65 and 84 weeks. In male mice, fatty change and fibrosis were evident at 22 weeks, and preneoplastic foci of altered hepatocytes were seen at an incidence of 8/8 (100%) and a multiplicity of 6.6 +/- 4.0 per mouse at 65 weeks. Hepatocellular adenomas and carcinomas developed at incidences of 16/24 (66.7%) and 5/24 (20.8%), and multiplicities of 1.42 +/- 1.32 and 0.29 +/- 0.62, respectively, at 84 weeks. The female mice exhibited resistance to development of these lesions. The CDAA diet also increased 8-OHdG levels in male but not female mice. These results indicate that a CDAA diet causes hepatocellular preneoplastic foci, adenomas and carcinomas associated with fibrosis and oxidative DNA damage in mice, as in rats, providing a hepatocarcinogenesis model caused by endogenous factors in mice.
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