Fig. 5

Copy number variations and somatic mutations between two angiogenesis subgroups. a A deletion of Chr 3 accompanied with an amplification of Chr 5 was enriched in all TCGA KIRC cases (upper panel). However these peaks in Chr 3 and Chr 5 did not differ significantly between the Cluster_1 and Cluster_2 angiogenesis subgroups (middle and lower panel); b only BAP1 showed significant mutation differences between two angiogenesis subgroups of TCGA KIRC patients; c GSEA showed that BAP1 in TCGA KIRC samples did not directly enriched in angiogenesis pathway, but significantly enriched in TP53, MYC target, hypoxia, epithelial mesenchymal transition (EMT), glycolysis, TGF-β signal related pathways; * represent P value less than 0.05; $ represent adjust P value less than 0.05