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. 2018 Mar 24;69(2):573–586. doi: 10.1002/hep.29792

Figure 6.

Figure 6

Abrogating ALK, FGFR2, and EphA5 activity leads to HCC patient–derived xenograft growth suppression. (A) Mice bearing HCC patient–derived xenograft model LI0752 were treated with vehicle or ceritinib (25 mg/kg), AZD4547 (12.5 mg/kg), or dasatinib (25 mg/kg) individually or in combination once a day for a consecutive 3 weeks. Tumor volume was measured twice a week. Bars represent means ± SEM, n = 6. (B) Tumor lysates were prepared and subjected to immunoblotting analysis with indicated antibodies. (C) Mice bearing HCC patient–derived xenograft model LI0752 were treated with vehicle or ganetespib (30 mg/kg or 50 mg/kg, three times per week). Tumor volume was measured twice a week. Bars represent means ± SEM, n = 6. (D) Tumor lysates were prepared and subjected to immunoblotting analysis with indicated antibodies. (E) A proposed overview of ALK, FGFR2 and EphA5 co‐activation in HCC cells and therapeutic strategies to block their activities were illustrated. Abbreviations: FRS2, FGFR substrate 2; GAPDH, glyceraldehyde 3‐phosphate dehydrogenase; T/C, treatment/control.