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. Author manuscript; available in PMC: 2016 Oct 31.
Published in final edited form as: Clin Cancer Res. 2015 Aug 13;21(24):5499–5510. doi: 10.1158/1078-0432.CCR-14-3091

Figure 3. p53 wild-type CRC tumors benefit from combined MEK- and mTOR- inhibition.

Figure 3

Mice bearing HT-29, HCT116 or LIM2405 tumors were treated with 3 consecutive doses of vehicle control (Control, C), PD901 (901, 2mg/kg, 6QD/W), MLN0128 (128, 0.3 mg/kg, 6QD/W) or the combination of both inhibitors (901+ 128). A. Tumors were collected and analyzed by western blot with the indicated antibodies. B. Tumors were collected and analyzed by immunohistochemistry with cleaved caspase 3 antibody. The images were quantified by a pathologist blinded to the identity of the samples. C. Mice bearing HT-29, HCT116, LIM2405, PDX-M6, PDX-T71, PDX-T72, PDX-T77, PDX-T96 were treated as indicated for 20–60 days. Measurements are displayed as mean ± S.E. D. Time on MEK- plus PI3K-therapy of 14 patients (blue) compared to the time on treatment for the previous chemotherapy-containing regimen (grey). The vertical line stands for the 16-week threshold (second response evaluation by computer tomography). The p53 status (sequencing and IHC) is provided in dark blue for wild-type p53, light blue for mutant p53 and shaded blue for non-available data. #, Patients exiting MEK- plus PI3K-therapeutic regimen because of toxicity.