Fig. 2

Transplanted Wnt1/iR1 tumors rapidly regress after inhibiting FGFR1 signaling following treatment with BGJ398. a Histological analysis of transplanted Wnt1/iR1 tumors as compared to spontaneous tumors. Upper panel: Hematoxylin and eosin (H&E) stain of spontaneous and transplanted Wnt1/iR1 tumors. Lower panel: Immunofluorescence double staining of luminal K8 (green) and basal K5 markers (red) in spontaneous and transplanted Wnt1/iR1 tumor sections. Nuclear staining is shown in blue (DAPI). b Immunofluorescence staining and quantification for vasculature using anti-CD31 in spontaneous and transplanted Wnt1/iR1 tumors; p = 0.51. c Immunofluorescence double staining for basal K5 (green) and HA epitope (red), and luminal K8 (green) and HA epitope (red) in spontaneous and transplanted Wnt1/iR1 tumor sections. Nuclear staining is shown in blue (DAPI) in all panels. d BGJ398 treatment scheme. e Tumor regression curve after receiving BGJ398 treatment, compared to control group treated with vehicle. Eleven mice in BGJ398 treatment group, four mice in vehicle treatment control group, 15 mice in total. f Immunofluorescence staining of the S phase proliferation marker BrdU, proliferative marker Ki67 and apoptotic marker cc3 in tumors from control and treatment groups (48 hours after BGJ398 treatment). g Quantification of immunofluorescence staining of nuclear BrdU, Ki67 and cc3 in tumor sections. BrdU (n ≥ 7): ****p < 0.0001; Ki67 (n ≥ 4): **p < 0.005; cc3 (n ≥ 6): **p < 0.005. Comparisons represent control versus 48 hours after BGJ398 treatment. Values are shown as mean ± SEM. BrdU Bromodeoxyuridine, cc3 Cleaved caspase 3, DAPI 4′, 6-Diamidino-2-phenylindole