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. Author manuscript; available in PMC: 2021 Apr 6.
Published in final edited form as: Sci Signal. 2020 Jun 16;13(636):eaay1451. doi: 10.1126/scisignal.aay1451

Fig. 3: Identification of apoptotic sensitizing compounds and drug targets in patient derived xenografts of colorectal cancer.

Fig. 3:

(A) Delta priming measurements of the top 35 hits from HT-DBP on seven PDX models of colorectal cancer and healthy cells Red indicates compounds that cause the highest increase in apoptotic priming. Dark blue indicates compounds that are less than 3 times standard deviation of DMSO treated wells. Data represent mean of 2 replicates. (B) Tumor volume after 21 days of in vivo treatment of COCA9 with navitoclax (100 mg/kg, p.o., daily), AT7519 (15 mg/kg, i.p., daily) or a combination of navitoclax and AT7519. Asterisk indicates a significant difference in tumor volume relative to vehicle treated cells (Mann-Whitney, p=0.03). Each point represents a single mouse; n = 4–5 mice per treatment arm. (C) Delta priming of the different PDX models based on nominal drug targets. Nominal targets include EGFR (31 compounds), pan-CDK (15 compounds), pan-HDAC (20 compounds), MEK (12 compounds), HSP90 (5 compounds). Data represent mean of 2 replicates. (D) Comparison of delta priming in COCA74P and COCA74M. Data represent mean of 2 replicates. (E) Delta priming of 17-DMAG for COCA74P and COCA74M. Each point represents an independent experiment. Lines represent mean of N = 2 experiments. (F) Delta priming of abexinostat for COCA74P and COCA74M. Each point represents an independent experiment. Lines represent mean of N = 2 experiments.