ArticlePloS one2008
Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 45 citations in OpenAlex.
- Targeting Chemical-induced Hepatocellular Carcinoma: Ameliorative Potential of Natural Compounds with Focus on Beta-carbolines.Mini reviews in medicinal chemistry · 2026Review
- Article
- Proliferative polyploid cells give rise to tumors via ploidy reduction.Nature communications · 2021Article
- Mice With Increased Numbers of Polyploid Hepatocytes Maintain Regenerative Capacity But Develop Fewer Hepatocellular Carcinomas Following Chronic Liver Injury.Gastroenterology · 2020Article
- In Vivo Lineage Tracing of Polyploid Hepatocytes Reveals Extensive Proliferation during Liver Regeneration.Cell stem cell · 2020Article
- Knockdown of Anillin Actin Binding Protein Blocks Cytokinesis in Hepatocytes and Reduces Liver Tumor Development in Mice Without Affecting Regeneration.Gastroenterology · 2018Article
- The Polyploid State Plays a Tumor-Suppressive Role in the Liver.Developmental cell · 2018Article
- Article
- Arid1a Has Context-Dependent Oncogenic and Tumor Suppressor Functions in Liver Cancer.Cancer cell · 2017Article
- FAM83H is involved in the progression of hepatocellular carcinoma and is regulated by MYC.Scientific reports · 2017Article
- c-MYC-Making Liver Sick: Role of c-MYC in Hepatic Cell Function, Homeostasis and Disease.Genes · 2017Review
- Hepatoblastoma modeling in mice places Nrf2 within a cancer field established by mutantJCI insight · 2016Article
- Enhanced angiogenesis, hypoxia and neutrophil recruitment during Myc-induced liver tumorigenesis in zebrafish.Scientific reports · 2016Article
- Oncogenic driver genes and the inflammatory microenvironment dictate liver tumor phenotype.Hepatology (Baltimore, Md.) · 2016Article
- Suppression of the SWI/SNF Component Arid1a Promotes Mammalian Regeneration.Cell stem cell · 2016Article
- Toxicity and carcinogenicity studies of Ginkgo biloba extract in rat and mouse: liver, thyroid, and nose are targets.Toxicologic pathology · 2014Article
- Inactivation of MYC reverses tumorigenesis.Journal of internal medicine · 2014Review
- MYC activation is a hallmark of cancer initiation and maintenance.Cold Spring Harbor perspectives in medicine · 2014Review
- Article
- Chronic inflammation, immune escape, and oncogenesis in the liver: a unique neighborhood for novel intersections.Hepatology (Baltimore, Md.) · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOverexpression of the human c-MYC (MYC) oncogene is one of the most frequently implicated events in the pathogenesis of hepatocellular carcinoma (HCC). Previously, we have shown in a conditional transgenic mouse model that MYC overexpression is restrained from inducing mitotic cellular division and tumorigenesis in the adult liver; whereas, in marked contrast, MYC induces robust proliferation associated with the very rapid onset of tumorigenesis in embryonic and neonatal mice. METHODOLOGY/PRINCIPAL
findingsHere, we show that non-genotoxic hepatotoxins induce changes in the liver cellular context associated with increased cellular proliferation and enhanced tumorigenesis. Both 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl(4)) cooperate with MYC to greatly accelerate the onset of liver cancer in an adult host to less than 7 days versus a mean latency of onset of over 35 weeks for MYC alone. These hepatotoxin-enhanced liver tumors grossly and histologically resemble embryonic and neonatal liver tumors. Importantly, we found that MYC overexpression is only capable of inducing expression of the mitotic Cyclin B1 in embryonic/neonatal hosts or adult hosts that were treated with either carcinogen. CONCLUSION/SIGNIFICANCE: Our results suggest a model whereby oncogenes can remain latently activated, but exposure of the adult liver to hepatotoxins that promote hepatocyte proliferation can rapidly uncover their malignant potential.
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.