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. 2021 May 27;142(2):339–360. doi: 10.1007/s00401-021-02327-x

Fig. 5.

Fig. 5

Targeting FGFR with tyrosine kinase inhibitors (FGFRis) impairs survival, clonogenicity and stem cell capacity of EPN cells. a Mean IC50 values, calculated from three independent experiments, of five different FGFRis (ponatinib, nintedanib, AZD-4547, dovitinib and erdafitinib) are depicted for the indicated cell models of different EPN subtypes in comparison to FGFR-positive (Hep3B, NCI-H1703) and negative (UW228 = MB SHH) controls. b Bar graphs depict fold changes of clonogenic survival upon treatment with the indicated FGFRi in comparison to untreated controls (set as 1) in PF-A (blue) and ST-RELA (pink) cell models. Cells were seeded at low density, exposed to the indicated drug concentrations and followed for 14 days. Hep3B and NCI-H1703 served as positive controls. c six days after treatment with the indicated inhibitors, spheres were seeded back into medium containing FCS and the capacity to attach and re-grow was followed. Results are presented as mean ± SD in comparison to untreated controls, set as 1. b, c Every value was evaluated from two independent experiments performed in duplicates and represented as mean ± SD. For b and c statistical differences between untreated and drug-exposed samples were determined by one-way ANOVA with Tukey correction for multiple comparison. n.r., not reached, ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05