Fig. 2: IFNγR2- and Jak1-mutant tumors are spontaneously controlled in vivo. | Nature Communications

Fig. 2: IFNγR2- and Jak1-mutant tumors are spontaneously controlled in vivo.

From: Tumor heterogeneity and clonal cooperation influence the immune selection of IFN-γ-signaling mutant cancer cells

Fig. 2: IFNγR2- and Jak1-mutant tumors are spontaneously controlled in vivo.

a Tumor growth curves of WT, IFNγR2-, and Jak1-mutant tumors. n = 10 mice; data are pooled from two independent experiments. b, c Representative histogram showing restored IFN-γ signaling after retroviral reintroduction of IFNγR2 (b) or Jak1 (c). Tumor cells were stimulated with 10 ng/mL IFN-γ for 16 h and measured for H-2Kb upregulation by flow cytometry. n = 4 stimulations; data is representative of two independent experiments. d, e Restoration of progressive tumor growth of IFNγR2 Mut.1 tumors with reintroduced IFNγR2 (d) and Jak1 Mut.1 tumors with reintroduced Jak1 (e). n = 15 mice (WT EV, IFNγR2 Mut.1, and IFNγR2 Mut.1 + IFNγR2), n = 10 mice (Jak1 Mut.2), n = 5 mice (Jak1 Mut.2 + Jak1); data are pooled from three (d) or one (e) independent experiments. Results are expressed as mean ± s.e.m. Statistical significance was determined by a two-way ANOVA Bonferroni post-hoc test (a, d, e). *** p < 0.001.

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