Extended Data Fig. 8: Mutational signatures impacting cancer cell-intrinsic signaling.
From: Ovarian cancer mutational processes drive site-specific immune evasion

a, Heatmap of scaled marker gene expression (averaged per cluster) for cancer cell clusters, showing differentially expressed genes in columns and clusters in rows. Genes are grouped by cluster. Top 5 genes per cluster are highlighted. b, Relative entropy of cell type subclusters to identify patient-specific clusters. c, Single cell distributions of PROGENy pathway activity per patient. d, Single-cell distributions of PROGENy pathway activity per cancer cell cluster (top subpanel), and as a function of HR status across all clusters (bottom subpanel). e, Heatmap of average HLA gene expression across clusters in adnexal, non-adnexal and ascites samples. f, Single cell distributions of HLA class II and class II gene expression per patient. g, Single cell distributions of HLA gene expression per cancer cell cluster (top subpanel), and as a function of HR status across all clusters (bottom subpanel). h, CD274 (PD-L1) gene expression in UMAP space (left) and as box plot distributions (right) with respect to cluster and mutational signature respectively. i, Dimensionality reduction of the dissimilarity in cancer cell cluster composition between pairs of samples using NMDS. Convex hulls highlight differences between samples based on the anatomic site and mutational signature. Size indicates the Shannon entropy in cluster composition per sample. In c, d and f–h, box plots show the median, top and bottom quartiles; whiskers correspond to 1.5× IQR. Paired brackets in d and g show two-sided Wilcoxon pairwise tests. Group comparisons in d, g and h show one-sided Wilcoxon test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.