Extended Data Fig. 8: AMG 510 treatment induces a pro-inflammatory tumour microenvironment.
From: The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumour immunity
a, CT-26 KRASG12C tumours were immunophenotyped by flow cytometry. Data are mean ± s.d., n = 8 mice per group; ****P < 0.0001, *P < 0.05; NS, not significant; one-way ANOVA followed by Tukey’s multiple-comparison test. MEKi, MEK inhibitor. b, Mice bearing CT-26 KRASG12C tumours were treated orally with a single dose of vehicle (black bar) or with the indicated dose of MEK inhibitor (blue bar). Tumours were collected 2 h later and levels of p-ERK were measured. MEK inhibitor concentrations in plasma (red triangle) or tumours (black open circle). Data are mean ± s.e.m., n = 3 mice per group; ****P < 0.0001 compared with vehicle; one-way ANOVA followed by Dunnett’s multiple-comparison test. c, Mice bearing CT-26 KRASG12C tumours were treated with MEK inhibitor at the indicated doses. Data are mean ± s.e.m., n = 8 mice per group; **** P < 0.0001 compared with vehicle; repeated-measures ANOVA followed by Dunnett’s multiple comparison test. d, Tumour volumes from the immunophenotyping study (a) of CT-26 KRASG12C tumour-bearing mice treated over 4 days. n = 8 mice per group. e, RNA was isolated from CT-26 KRASG12C tumours. n = 5 mice per group. Gene expression and scores were calculated by nSolver v.4.0. Data are mean ± s.d.; ****P < 0.0001, ***P < 0.001, ** P < 0.01, *P < 0.05; NS, not significant; one-way ANOVA followed by Tukey’s test.
