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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Mol Cancer Res. 2009 Nov 24;7(12):1937–1945. doi: 10.1158/1541-7786.MCR-09-0333

Figure Four.

Figure Four

Bmi1 cooperates with activated Ras (RasV12) to promote hepatic carcinogenesis in vivo. (A) Tumor development incident curves in mice. The cumulative hazard represents the relative probability of tumor development in each condition; (B) Representative gross image of liver tumors induced by Bmi1/RasV12. Arrows indicate visible tumor nodules; (C) Quantitative RT-PCR analysis of AFP expression in normal liver and Bmi1/RasV12 tumor samples; (D) H&E staining of non-tumor liver (NT) and HCC (T) induced by Bmi1/RasV12 (upper). Immunohistochemical staining with anti-V5 antibody showing staining of V5-tagged Bmi1 in HCC cells in a tumor nodule, with sporadic staining in non-tumor liver tissues (middle). Insets: expanded view showing specific nuclear staining of Bmi1 in non-tumor liver or HCC cells. Immunohistochemical staining of phospho-ERK in both NT and T samples (lower); (E) Western blot analysis of N-Ras, phospho-ERK, and ERK expression. Actin was used as loading control.