Figure 3.
Tumor growth inhibition and induction of apoptosis in RS1316 SC model treated with Duv, Ven and their combination. (A) Experimental design: RS1316 cells were SC injected and left to engraft. Mice were randomized in 4 treatment groups, treated for 5 consecutive days, and euthanized at the same time point. (B) Pictures of tumor masses (left) and summary graph of their volume (right) at the end of the experiment. Data are reported as mean ± SEM. (C) Quantification of cleaved (Cl.) Caspase-3 signal, obtained by immunohistochemistry performed on tumor masses, represented as percentage of positive area. Data are reported as mean ± SEM. (D) Hematoxylin/eosin (H/E, ×20) and cleaved (Cl.) Caspase-3 IHC staining (magnification ×40). Veh: vehicle. Statistical analysis was performed using 1-way ANOVA; *P < .05, **P < .01, ***P < .001, ****P < .0001.

Tumor growth inhibition and induction of apoptosis in RS1316 SC model treated with Duv, Ven and their combination. (A) Experimental design: RS1316 cells were SC injected and left to engraft. Mice were randomized in 4 treatment groups, treated for 5 consecutive days, and euthanized at the same time point. (B) Pictures of tumor masses (left) and summary graph of their volume (right) at the end of the experiment. Data are reported as mean ± SEM. (C) Quantification of cleaved (Cl.) Caspase-3 signal, obtained by immunohistochemistry performed on tumor masses, represented as percentage of positive area. Data are reported as mean ± SEM. (D) Hematoxylin/eosin (H/E, ×20) and cleaved (Cl.) Caspase-3 IHC staining (magnification ×40). Veh: vehicle. Statistical analysis was performed using 1-way ANOVA; *P < .05, **P < .01, ***P < .001, ****P < .0001.

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