Fig. 3.
HCC development is attenuated by hepatocyte-specific inactivation of Cdk2. Cdk2f/f (n = 9) and Cdk2Δhepa (n = 8) mice were treated with DEN at the age of 14 d and euthanized at the age of 40 wk. (A) Cdk2 deletion efficiency in the liver (Δhepa) was verified by PCR using hepatic cDNA and by immunoblot (IB). (B) Macroscopic appearance of representative livers from 40-wk-old Cdk2f/f and Cdk2Δhepa animals. (C) Scatter plots showing the number of macroscopic HCC nodules per mouse (Left), cumulative tumor diameter (mm, Middle) and liver:body weight ratio (%, Right) for each animal. (D) Gene expression analysis of cyclin E1 (Left), cyclin E2 (Middle), and cyclin A2 (Right) in livers of DEN-treated Cdk2f/f (n = 9) and Cdk2Δhepa (n = 8) animals. Expression levels were calculated as fold induction in comparison with untreated WT controls (Cdk2f/f ctrl, n = 3). *P < 0.05; **P < 0.005.