Fig. 7

Transcriptomic analyses of SR PDX models. a Expression of EGFR ligands in untreated control tumors of the different response groups. CR, complete response, PR, partial response, SD, stable disease, PD, progressive disease. b Enrichment plots from GSEA for CET-sensitive compared to resistant PDX tumors showing an enrichment of the hallmark KRAS signaling-up gene set. c DUSP6 expression fold change relative to untreated control tumors in SR PDX models with and without driver gene mutations compared to the corresponding CET-sensitive tumors treated for 5 days (5dC). Fold changes were calculated as mean values from at least three measurements. The line indicates the mean. *, models with KRAS_SIGNALLING_UP” set found to be enriched. d DUSP6 expression in PDX models correlated with driver mutation and KRAS gene set enrichment status. e Upregulation of genes involved in the PI3K-AKT and/or RAS pathway, selected from KEGG pathways. The line indicates the mean. Mann-Whitney U was used to determine significance. 5dC, tumors treated for 5 days with CET and still sensitive to CET. C, tumors with SR under chronic CET treatment