Skip to main content
. Author manuscript; available in PMC: 2014 Aug 20.
Published in final edited form as: Clin Cancer Res. 2014 Apr 11;20(11):2947–2958. doi: 10.1158/1078-0432.CCR-13-3448

Figure 4.

Figure 4

Blockade of IGF-I–induced IGF-IR and hybrid receptor signaling in human ovarian cancer xenografts by ganitumab. Mice bearing OV-90 or TOV-21G xenografts between 300 and 450 mm3 (n= 3 per group) were injected intraperitoneally with 1 mg ganitumab or hIgG1. After 6 hours, IGF-I (5 µg) or 1× PBS was administered intravenously, and after 15 minutes, xenografts were collected and analyzed for levels of phosphorylated IGF-IR, INSR, and AKT. A, ganitumab inhibited IGF-IR and AKT but not INSR phosphorylation in OV-90 xenografts. B, ganitumab did not inhibit IGF-IR, INSR, and AKT phosphorylation in TOV-21G xenografts. Data, mean ± SEM. Student t test was used to determine whether ganitumab significantly nhibited the activation of IGF-IR, INSR, or AKT when compared with hIgG1 control. *, P < 0.01.