Fig. 5

Co-blockade of PDGFRβ with MEK-JAK inhibition enhances tumor cell killing via intratumoral T-cells in vivo. a 6-week-old female BALB/c nude mice cohorts were injected in the 4th inguinal mammary fat pad with the MDA-MB-231 cells line. Mice were treated with vehicle, MEK162 (5 mg/kg), NVP-BSK805 (50 mg/kg), Nilotinib (37.5 mg/kg) individually or in combination for 14 days. Tumor size (area, mm²) was measured using a digital calliper and mean tumor size of each cohort is presented. Graph represents the mean tumor area ± SEM from six mice/group (****P ≤ 0.0001). b Survival of mice of panel a was monitored over the indicated period of time and the statistical significance of data was analyzed by log-rank test (P < 0.0001); n = 6 mice/group. c Similarly to panel a, syngeneic mammary carcinoma cell line 4 T1.2 model was established using 6-week-old female BALB/c mice and tested with indicated inhibitors. Graph represents the mean tumor area ± SEM from six mice/group (****P ≤ 0.01). d Representative images of gross morphology of excised tumor are shown for panel c. e Representative images of ApopTag staining in tumors treated with vehicle and triple-combination therapy. f, g Percentage of viable immune cells infiltrates gated using indicated antibodies as shown in Additional file 8: Figure S7F in both spleens and tumor tissues isolated from indicated treatment groups. Graph represents each cell population from six mice/group± SEM (*P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001). h Syngeneic 4 T1.2 cancer model as in panel c was established and treated singly or in combination with anti-CD8 or triple-combination. Tumor size (area, mm²) was measured using a digital caliper and mean tumor size of each cohort is presented. Graph represents the mean tumor area ± SEM from six mice/group (***P ≤ 0.001)