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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Differential responses to immune checkpoint inhibitor dictated by pre-existing differential immune profiles in squamous cell carcinomas caused by same initial oncogenic drivers

Fig. 3

Bulk RNA-seq data of TAb2 and TCh3 tumors that differ significantly in their gene transcription and WES data of TAb2 and TCh3 tumors. A Volcano plot of differentially expressed genes (DEG) between TCh3 (blue) and TAb2 (red) tumors. Difference between DEGs in these two groups was plotted against a threshold of log2(fold change) = 2 and Benjamini-Hochberg (BH) adjusted p-value = 0.05. B Heatmap of gene expression of selected cytokines and chemokines. Expression values for each gene are scaled across TAb2 (n = 2) and TCh3 (n = 2) tumor cells. Genes were filtered for those differentially expressed with a threshold of log2(fold change) = 2 and BH adjusted p-value = 0.05. C-E Ingenuity Pathway Analysis (IPA) of the altered genes for corresponding pathways to identify the canonical pathways that were significantly enriched among the DEGs in TAb2 and TCh3 tumors. The key affected pathways, components, and cellular functions of the TME are presented in (C) tumor-secreted factors, (D) cytoplasm, and (E) nucleus of TAb2 tumors compared to TCh3 tumors. Prediction legend indicates the measurement in dataset, predicted activation or inhibition, and predicted relationships. F WES data showing TAb2 and TCh3 tumors exhibited genetic differences. Total numbers of tumor-specific somatic mutations in TAb2 or TCh3 tumors analyzed by two pipelines GATK (left) and BCFtools (right). Mutation type abbreviations: MV: Missense Variant; SDV: Splice Donor Variant; IV: Intron Variant; SG: Stop Gained; FV: Frameshift Variant; SL: Start Lost; SRV: Splice Region Variant; SAV: Splice Acceptor Variant; 5PUV: 5 Prime UTR Variant; CID: Conservative Inframe Deletion

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