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. 2021 Mar 24;19:39. doi: 10.1186/s12964-021-00728-9

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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