Fig. 2From: Inflammatory response-based prognostication and personalized therapy decisions in clear cell renal cell cancer to aid precision oncologyIdentification of three inflammatory response subtypes with diverse immunological features, clinical outcomes, and genomic alterations in TCGA-KIRC dataset. A Circos track plots illustrate genomic location, interactions, and prognostic relevance of inflammatory response genes. In the inner circle, protein–protein interactions are displayed. Blue dots denote univariate cox regression analysis-derived HR > 1, and red dots denote HR < 1. In the outer circle, genomic location of each inflammatory response gene is shown. B Consensus matrix k = 3. Colors from white to blue denote never cluster together to always cluster together. C PCA demonstrates the subtype assignments utilizing transcriptome profiles. D K-M curves of OS among three inflammatory response subtypes. E Transcriptional levels of common immune checkpoint molecules, abundance of immune and stromal cell types, and immune and stromal scores across the three subtypes. F Activity of oncogenic hallmark pathways and clinicopathological features in the three subtypes. G Differences in clinicopathological parameters among the three subtypes. H Sankey diagram illustrates the interactions of inflammatory response subtypes with known immune subtypes. I The mutational waterfall among the three inflammatory response subtypes. Mutated genes are ranked by mutational frequency. J Differences in the fractions of genome altered, amplification and deletion among the three subtypes. * p < 0.05. (K-M) Detection and comparison of significant copy-number amplifications and deletions across the three subtypesBack to article page