Skip to main content
Figure 3 | Journal of Translational Medicine

Figure 3

From: The AKT inhibitor AZD5363 is selectively active in PI3KCA mutant gastric cancer, and sensitizes a patient-derived gastric cancer xenograft model with PTEN loss to Taxotere

Figure 3

Pharmacodynamic study of tumors treated with AZD5363 or in combination with Taxotere. (A) and (B). Suppression of AKT downstream signalling by AZD5363 in SGC100 PDGCX tumors with PI3KCA muttion. The tumor bearing mice were treated with AZD5363 (150 mg/kg, bid) for 25 days. Tumors samples were collected two hours post-final dose and were subjected to western blot analysis for phospho-AKT (S473), phospho-PRAS40 (T246) and phosphor S6 (A). The expression levels were quantified by gel imaging scan and expressed as mean + SD (B). (C) and (D). Mudulation of AKT downstream signalling by AZD5363 and Taxotere in SGC020 PDGCX tumors with PTEN loss. The tumor bearing mice were treated with AZD5363 (150 mg/kg, bid) in combination with Taxotere (5 mg/kg weekly) for 25 days. Tumors samples were collected two hours post-final dose and were subjected to western blot for phospho-AKT (S473), phospho-PRAS40 (T246) and phosphor S6 (C). The expression levels were quantified by gel imaging scan and expressed as mean + SD (D). Students’ t-tests were used to compare modulation in the treatment group with the control group. Statistical tests were two sided, with P < 0.05 considered significant (*).

Back to article page