ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Molecular mechanisms of fibrosis-associated promotion of liver carcinogenesis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 106 citations in OpenAlex.
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- Impact of nucleos(t)ide analogues on the risk of hepatocellular carcinoma in chronic hepatitis B patients: a time-dependent Cox regression analysis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2025Article
- Oncogenic plasmid DNA and liver injury agent dictates liver cancer development in a mouse model.Clinical science (London, England : 1979) · 2024Article
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- SPINK1-induced tumor plasticity provides a therapeutic window for chemotherapy in hepatocellular carcinoma.Nature communications · 2023Article
- Combined, elobixibat, and colestyramine reduced cholesterol toxicity in a mouse model of metabolic dysfunction-associated steatotic liver disease.Hepatology communications · 2023Article
- BEX1 supports the stemness of hepatoblastoma by facilitating Warburg effect in a PPARγ/PDK1 dependent manner.British journal of cancer · 2023Article
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- DNASE1L3 inhibits hepatocellular carcinoma by delaying cell cycle progression through CDK2.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Hepatic SIRT6 deficit promotes liver tumorigenesis in the mice models.Genes & diseases · 2022Article
- Mouse Models of Hepatocellular Carcinoma: Classification, Advancement, and Application.Frontiers in oncology · 2022Review
- In Vivo and In Vitro Models of Hepatocellular Carcinoma: Current Strategies for Translational Modeling.Cancers · 2021Review
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Hepatocellular carcinoma (HCC) mostly develops in patients with advanced fibrosis; however, the mechanisms of interaction between a genotoxic insult and fibrogenesis are not well understood. This study tested a hypothesis that fibrosis promotes HCC via a mechanism that involves activation of liver stem cells. First, B6C3F1 mice were administered diethylnitrosamine (DEN; single ip injection of 1mg/kg at 14 days of age). Second, carbon tetrachloride (CCl(4); 0.2ml/kg, 2/week ip starting at 8 weeks of age) was administered for 9 or 14 weeks to develop advanced liver fibrosis. In animals treated with DEN as neonates, presence of liver fibrosis led to more than doubling (to 100%) of the liver tumor incidence as early as 5 months of age. This effect was associated with activation of cells with progenitor features in noncancerous liver tissue, including markers of replicative senescence (p16), oncofetal transformation (Afp, H19, and Bex1), and increased "stemness" (Prom1 and Epcam). In contrast, the dose of DEN used did not modify the extent of liver inflammation, fibrogenesis, oxidative stress, proliferation, or apoptosis induced by subchronic CCl(4) administration. This study demonstrates the potential role of liver stem-like cells in the mechanisms of chemical-induced, fibrosis-promoted HCC. We posit that the combination of genotoxic and fibrogenic insults is a sensible approach to model liver carcinogenesis in experimental animals. These results may contribute to identification of cirrhotic patients predisposed to HCC by analyzing the expression of hepatic progenitor cell markers in the noncancerous liver tissue.
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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.