Document Detail


A novel mouse model of hepatocarcinogenesis triggered by AID causing deleterious p53 mutations.
MedLine Citation:
PMID:  18997814     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
A Takai; T Toyoshima; M Uemura; Y Kitawaki; H Marusawa; H Hiai; S Yamada; I M Okazaki; T Honjo; T Chiba; K Kinoshita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-11-10
Journal Detail:
Title:  Oncogene     Volume:  28     ISSN:  1476-5594     ISO Abbreviation:  Oncogene     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-01-30     Completed Date:  2009-02-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  469-78     Citation Subset:  IM    
Affiliation:
Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
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MeSH Terms
Descriptor/Qualifier:
Aging / genetics,  metabolism
Alkaline Phosphatase / genetics,  metabolism*
Animals
Antigens, Differentiation / genetics,  metabolism
B-Lymphocytes / metabolism,  pathology
Carcinoma, Hepatocellular / genetics,  metabolism*,  pathology
Cytidine Deaminase / genetics,  metabolism*
Disease Models, Animal
Embryo, Mammalian / metabolism,  pathology
Gene Expression Regulation, Neoplastic* / genetics
Genome, Human / genetics
Hepatitis / genetics,  metabolism,  pathology
Humans
Liver / metabolism,  pathology
Liver Neoplasms / genetics,  metabolism*,  pathology
Mice
Mice, Transgenic
Organ Specificity / genetics
Sequence Deletion / genetics
Somatic Hypermutation, Immunoglobulin / genetics
Stem Cells / metabolism,  pathology
Tumor Suppressor Protein p53 / genetics,  metabolism*
alpha-Fetoproteins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Antigens, Differentiation; 0/Tumor Suppressor Protein p53; 0/alpha-Fetoproteins; EC 3.1.3.1/Alkaline Phosphatase; EC 3.5.4.-/AICDA (activation-induced cytidine deaminase); EC 3.5.4.5/Cytidine Deaminase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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