Author/Authors :
Lou، نويسنده , , Dan-Qing and Molina، نويسنده , , Thierry and Bennoun، نويسنده , , Myriam and Porteu، نويسنده , , Arlette and Briand، نويسنده , , Pascale and Joulin، نويسنده , , Virginie and Vasseur-Cognet، نويسنده , , Mireille and Cavard، نويسنده , , Catherine، نويسنده ,
Abstract :
We closely mimicked the in vivo setting in which sporadic hepatocarcinoma occurs by establishing a transgenic mouse model carrying regulatable SV40 early sequences under the control of the regulatory sequences of the human antithrombin III gene that confer hepatic expression. In this system, floxed dormant oncogenic sequences became functional after excision due to adenoviral expression of Cre recombinase or the stable transgenic expression in liver of a tamoxifen-inducible Cre. Hepatic oncogene expression was switched on by both methods, leading to the development of hepatocellular carcinoma. This model could be useful for investigating the key steps of the preneoplastic process, to identify suitable targets for the testing of new therapies.
Keywords :
Cre recombinase , Tamoxifen , hepatocellular carcinoma , SV40 large T antigen , Transgenic