FIGURE 3 from Reshaping the Tumor Microenvironment of KRASG12D Pancreatic Ductal Adenocarcinoma with Combined SOS1 and MEK Inhibition for Improved Immunotherapy Response

scRNA-seq reveals tumor-intrinsic mechanisms and cellular and molecular cross-talk in the TME in response to SOS1i+MEKi treatment. A, Experiment design of scRNA-seq experiments. B, UMAP visualization (left) of 153,678 KPCY TME cells from n = 20 mice across all conditions (TC3, TC4, and TC5 TME after treatment of vehicle or SOS1i+MEKi). Major cell types identified through graph-based clustering are indicated by color. Heat map (right) showing the relative average expression of common cell type–specific marker genes for each cluster for annotation. C, Bar graph showing cell proportion/composition of indicated cell type in the TME of each mouse (mean ± 95% confidence interval). D, Pathway enrichment analysis of upregulated and downregulated genes in epithelial/tumor cells in response to SOS1i+MEKi treatment across all mice (n = 20). E, Dot plot showing gene expression of Cxcl9, Cxcl10, and Ccl3 across conditions.