ArticleOncogene2009
A novel mouse model of hepatocarcinogenesis triggered by AID causing deleterious p53 mutations.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 66 citations in OpenAlex.
- Epigenetic activation of JAG1 by AID contributes to metastasis of hepatocellular carcinoma.The Journal of biological chemistry · 2025Article
- Adenosine, bridging chronic inflammation and tumor growth.Frontiers in immunology · 2023Review
- Cancer-inducing niche: the force of chronic inflammation.British journal of cancer · 2022Review
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- The immunological and metabolic landscape in primary and metastatic liver cancer.Nature reviews. Cancer · 2021Review
- Review
- Caspase-1 from Human Myeloid-Derived Suppressor Cells Can Promote T Cell-Independent Tumor Proliferation.Cancer immunology research · 2018Article
- Potential therapeutic targets ofOncotarget · 2018Review
- Involvement of activation-induced cytidine deaminase in skin cancer development.The Journal of clinical investigation · 2016Article
- Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.Nature reviews. Immunology · 2016Review
- Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis.Neoplasia (New York, N.Y.) · 2016Article
- Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma.Frontiers in chemistry · 2016Review
- Associations between activation-induced cytidine deaminase/apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like cytidine deaminase expression, hepatitis B virus (HBV) replication and HBV-associated liver disease (Review).Molecular medicine reports · 2015Review
- AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway.EMBO molecular medicine · 2015Article
- Development of a High-Throughput Molecular Imaging-Based Orthotopic Hepatocellular Carcinoma Model.Cureus · 2015Article
- Article
- Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- Hsa-miR-520d induces hepatoma cells to form normal liver tissues via a stemness-mediated process.Scientific reports · 2014Article
- Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms.Nature reviews. Cancer · 2013Review
- APOBEC3 cytidine deaminases in double-strand DNA break repair and cancer promotion.Cancer research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID), the only enzyme that is known to be able to induce mutations in the human genome, is required for somatic hypermutation and class-switch recombination in B lymphocytes. Recently, we showed that AID is implicated in the pathogenesis of human cancers including hepatitis C virus (HCV)-induced human hepatocellular carcinoma (HCC). In this study, we established a new AID transgenic mouse model (TNAP-AID) in which AID is expressed in cells producing tissue-nonspecific alkaline phosphatase (TNAP), which is a marker of primordial germ cells and immature stem cells, including ES cells. High expression of TNAP was found in the liver of the embryos and adults of TNAP-AID mice. HCC developed in 27% of these mice at the age of approximately 90 weeks. The HCC that developed in TNAP-AID mice expressed alpha-fetoprotein and had deleterious mutations in the tumour suppressor gene Trp53, some of which corresponded to those found in human cancer. In conclusion, TNAP-AID is a mouse model that spontaneously develops HCC, sharing genetic and phenotypic features with human HCC, which develops in the inflamed liver as a result of the accumulation of genetic changes.
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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.