Fig 1: Ligand-receptor interactions in the VS-TME distinguish Injury-like from nmSC Core tumors, and promote myeloid cell proliferation and migration.a Bar plot showing the relative information flow of select signaling pathways. Pathway names in red are enriched in Injury-like VS and those in blue are enriched in Core VS. Information flow is defined as the sum of communication probability among all pairs of cell groups in each inferred network. See Supplementary Data 9. b Heatmap showing relative expression of VS-SC ligands (left) with receptors expressed on myeloid cells (right). c Box-and-whisker plots showing the mean log-normalized expression of candidate ligands in VS-SC from Fig. 5b. CSF1 expression is higher in Injury-like VS (two-sided t-test, multiple testing correction with Benjamini Hochberg Method and FDR of 20%. Inury-like (n = 6) and nmSC Core (n = 5) groups defined in (a). Center lines of the boxplots reflect the mean, upper and lower borders reflect the 75th and 25th percentiles, respectively, whiskers are the highest and lowest points at most 1.5 times the inter-quartile range from the hinge, and outliers are represented as dots. See the Source Data file for exact values. d Bar plots showing relative proliferation (left) and transwell migration (right) of CD14+ monocytes from healthy donors in Basal Media (BM), HSC Conditioned Media (CM), CM with isotype IgG control, and CM with anti-CSF1. Each bar represents the normalized mean of all technical replicates (n = 3 per assay) across biological replicates (n = 3) and error bars are SEM. e Model of Injury-like VS. VS-SC undergo a critical stressor that triggers subpopulations to adopt repair-like and antigen presenting states. Myeloid cells are recruited to the VS TME and proliferate locally, leading to tumor progression. Source data are provided as a Source Data file.