Figure 5 from KRAS Inhibitor–Induced Cancer Cell Death Enhances Sensitivity to Immune-Mediated Bystander Killing of Drug-Resistant Subclones

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Treatments modulate the immune TME and increase inflammation. A, Schematic: Mixed subcutaneous tumors (BFP KRAS G12C cells plus 0.2% Luc-eGFP KRAS G12D cells) were treated for 6 days with RMC-4998 (G12Ci) ± RMC-4550 (SHP2i) or anti–PD-1 (aPD-1). Flow cytometry of tumors and tdLNs was performed. For all subsequent plots, each dot represents one individual tumor; mean ± SD; one-way ANOVA Kruskal–Wallis test comparing vehicle with each treatment or G12Ci with combination treatments (only significant comparisons). B, Fraction of KRAS G12C (left) and KRAS G12D (right) cells of all live cells. C, Fraction of macrophages (MP) of all immune cells (CD45+). D, Macrophage polarization: fraction of Arg1high MHC-IIlow (left) and Arg1low MHC-IIhigh (right) MPs of all MPs. E, Fraction of CD8+ T cells of CD45+ cells. F, Fraction of NK cells of CD45+ cells. G, CD8+ T-cell/Treg (CD4+ Foxp3+ T cells) ratio. H, Fraction of Tem (CD44+/CD62L−; left) and TIM3high Lag3high (right) CD8+ T cells of CD45+ cells. I, In tdLN, fraction of Tem (CD44+/CD62L−) CD8+ T cells of all CD8+ T cells. *, P < 0.05, **, P < 0.01: ***, P < 0.001, ***, P < 0.0001.

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