Fig. 6: Tumor suppressive effects of a combination of other RTK pathway inhibitors and prednisone in xenograft studies. | Nature Communications

Fig. 6: Tumor suppressive effects of a combination of other RTK pathway inhibitors and prednisone in xenograft studies.

From: Comprehensive targeting of resistance to inhibition of RTK signaling pathways by using glucocorticoids

Fig. 6

a–e N = 6 mice per group. Ten million KRAS and ATM mutant H23 lung cancer cells, 5 million PDGFR amplification H1703 lung cancer cells, 1 million BRAF V600E mutant A2058 melanoma cells, 2 million ERBB2 amplification esophageal adenocarcinoma (gastric cancer) OE19 cells, and 5 million FGFR mutant RT112 bladder cancer cells were s.c. injected to 24 mice for each line. After tumor formation, mice were treated with the indicated drug for the indicated days. Trametinib is a MEK inhibitor and H23 is sensitive to it. Imatinib is a BCR-ABL/PDGFR inhibitor and H1703 is moderately sensitive/resistant. Vemurafenib targets BRAF V600E but A2058 is completely resistant. Lapatinib is an ERBB2 inhibitor and OE19 is sensitive. Infigratinib is an FGFR1-3 inhibitor under clinical trials and RT112 is sensitive. Lower dose (1 mg/kg/day) or higher dose (100 mg/kg/day) RTK inhibitors were used based on the initial sensitivities of these different cell lines. Representative tumor photos were shown. Tumor sizes were measured by a caliper and shown as mean volume ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, by repeated measures (RM) two-way ANOVA, adjusted by Bonferroni’s test. The statistical analysis above was performed on Graphpad Prism 9.0.0. Source data are provided as a Source Data file. p = 0.002,0.05,0.004,0.03,0.04.

Back to article page