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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Adenovirus-mediated gene therapy in a mouse model of hereditary tyrosinemia type I.

Mice lacking the enzyme fumarylacetoacetate hydrolase (FAH) have symptoms similar to humans with the disease hereditary tyrosinemia type I (HT1). FAH-deficient mice were injected with a first-generation adenoviral vector expressing the human FAH gene and followed for up to 9 months. Nontreated FAH mutant control mice died within 6 weeks from fulminant liver failure, whereas FAH adenovirus-infected animals survived until sacrifice at 2-9 months. Nine of 13 virus-treated animals developed hepatocellular cancer. Immunohistochemical analysis revealed a mosaic of FAH-deficient and FAH-positive cells in all animals and liver function tests were improved compared to controls. Even mice harvested 9 months after viral infection had > 50% FAH-positive cells. These results demonstrate the strong selective advantage of FAH-expressing cells in an FAH-deficient liver but also illustrate the danger of carcinomas arising from FAH-deficient hepatocytes in HT1.[1]


  1. Adenovirus-mediated gene therapy in a mouse model of hereditary tyrosinemia type I. Overturf, K., al-Dhalimy, M., Ou, C.N., Finegold, M., Tanguay, R., Lieber, A., Kay, M., Grompe, M. Hum. Gene Ther. (1997) [Pubmed]
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