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. Author manuscript; available in PMC: 2018 Aug 14.
Published in final edited form as: Nature. 2018 Feb 14;554(7693):544–548. doi: 10.1038/nature25501

Extended Data Figure 4. Contrasting Lund and TCGA molecular subtyping.

Extended Data Figure 4

a, Tumour mutation burden (TMB; y-axis) is plotted against Lund and TCGA subtypes (x-axis). The Lund genomically unstable (two-tailed t test; p = 0.00018) and TCGA luminal II subtypes (p = 0.00024) have a higher median TMB. b, Patients are split into TMB low (grey) and high (black), based on median TMB, and the fraction of patients in these two groups is shown for the Lund and TCGA molecular subtypes. c–e, TGF-β as likely driver of differential response in Lund GU. c, Three patient subgroups: Lund GU but not TCGA luminal II, both GU and luminal II, or luminal II but not GU. d, CD8+ Teff, Pan-F-TBRS and TMB by subgroup. e, Response differs significantly by subgroups (two-tailed Fisher exact p = 0.00062). The numbers above the graphs or in parentheses specify sample numbers in each bin. GU, genomically unstable; Inf, infiltrated; Pan-F-TBRS: pan-tissue fibroblast TGF-β response genes; SCCL, basal/SCC-like; Teff: CD8 T effector signature; TMB: tumour mutation burden; UroA, urothelial-like A; UroB, urothelial-like B.