1997
DOI: 10.1002/(sici)1520-670x(1997)10:2<135::aid-jtra11>3.0.co;2-s
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LEC rats: An overview of recent findings

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Cited by 13 publications
(4 citation statements)
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References 43 publications
(48 reference statements)
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“…The reason for this discrepancy between rat and human seems to be dependent on their etiology. The LEC rat, which was previously investigated, spontaneously develops hereditary hepatitis and hepatoma as the result of an abnormality in copper metabolism, 32 while all patients with HCC enrolled in this study suffered from HCC after a long history of either hepatitis B or C virus infection. In LEC rats, the typical inflammatory cells are relatively few, although many oval cells that are thought to be stem cells for hepatocytes appear in nontumor tissue.…”
Section: Discussionmentioning
confidence: 99%
“…The reason for this discrepancy between rat and human seems to be dependent on their etiology. The LEC rat, which was previously investigated, spontaneously develops hereditary hepatitis and hepatoma as the result of an abnormality in copper metabolism, 32 while all patients with HCC enrolled in this study suffered from HCC after a long history of either hepatitis B or C virus infection. In LEC rats, the typical inflammatory cells are relatively few, although many oval cells that are thought to be stem cells for hepatocytes appear in nontumor tissue.…”
Section: Discussionmentioning
confidence: 99%
“…Although the exact onset of the disease varies, depending on the report, LEC rats spontaneously develop acute hepatitis at 12 to 24 weeks after birth, followed by chronic hepatitis (Miyoshi et al, 1997a). At 40 weeks of age, they begin to develop nodules in the liver which progress to hepatoma.…”
Section: Wiley-liss Incmentioning
confidence: 99%
“…The Long-Evans rats with a cinnamon-like coat colour (LEC rat) have already been identified as an excellent animal model for studying Wilson's disease (WD; Miyoshi et al 1997). These rats have a mutation in Atp7b that encodes P-type adenosine triphosphatase, a gene homologous to the WD gene (Wu et al 1994) and show some of the clinical features of the disease including hepatic copper (Cu) accumulation and reduced biliary Cu excretion.…”
Section: Introductionmentioning
confidence: 99%