Volume 62, Issue 2, Pages 257-259 (February 2015) Molecularly targeted therapies for human hepatocellular carcinoma: Should we start from β-catenin inhibition?  Diego F. Calvisi  Journal of Hepatology  Volume 62, Issue 2, Pages 257-259 (February 2015) DOI: 10.1016/j.jhep.2014.11.021 Copyright © 2014 European Association for the Study of the Liver Terms and Conditions

Fig. 1 Schematic representation of the protocol employed by Delgado et al. [15]. (A) Six-week old C3H/He male mice were injected intraperitoneally with the potent hepatocarcinogen diethylnitrosamine, followed 3weeks later by initiation of a diet containing 0.05% phenobarbital (DEN/PB). These mice developed liver tumours harbouring β-catenin mutations (β-catenin+ liver tumours). Of note, liver tumour development was completely suppressed by treatment with locked nucleic acid (LNA; red blunted arrow) against β-catenin in these mice. (B) A second group of C3H/He male mice was subjected to the administration of DEN only. These mice developed liver tumours harbouring Ha-Ras or B-Raf mutations (Ha-Ras+ or B-Raf+ liver tumours) but not β-catenin mutations. In these mice, tumour development was unaffected by administration of LNA against β-catenin. Journal of Hepatology 2015 62, 257-259DOI: (10.1016/j.jhep.2014.11.021) Copyright © 2014 European Association for the Study of the Liver Terms and Conditions