a, Landscape of driver mutations in CAC samples (n = 99) and dysplastic UC samples (n = 13). Genes with asterisks are drivers in CACs (Methods). CNAs of known oncogenes are depicted only for the 34 CACs that were newly analysed in this study. b, Frequency of driver mutations among clones identified in non-dysplastic samples from patients with UC (n = 183) versus sCRC samples from the Japanese cohort (n = 525). Asterisks indicate q < 0.1 (two-sided Fisher’s exact test with Benjamini–Hochberg adjustment). c, Number (middle) and relative frequency (bottom) of mutations allocated to signatures A and B in samples of single crypts from control individuals (n = 43) and non-dysplastic (n = 241; 58 single crypts and 183 clones), dysplastic (n = 13 clones) and non-hypermutated CAC (n = 92 samples) from patients with UC. Information about disease state, pathology and sample type is indicated at the top. d, Comparison of the number of mutations detected by WES in clones identified in non-dysplastic samples, dysplastic samples and CAC samples without hypermutation from patients with UC. Two-sided Mann–Whitney U test. e, Mutational signatures of colorectal epithelium from control individuals and patients with UC. f, Fraction of signature B mutations in single crypts from control individuals, and clones identified in non-dysplastic (ND), dysplastic (D) and non-hypermutated CAC samples containing ≥ 10 mutations from patients with UC. Two-sided Mann–Whitney U test. g, Box plots of the fractions of genomic regions that contain CNAs in clones identified in non-dysplastic (n = 183), dysplastic (n = 13) and CAC (n = 34) samples from patients with UC. Two-sided Mann–Whitney U test. h, Bottom, colour-gradient maps of CNAs and UPDs as detected by WES data are shown for clones identified in non-dysplastic (n = 183), dysplastic (n = 13) and CAC (n = 34) samples from patients with UC. Top, pathological grade, fractions of genomes that exhibit CNAs and UPDs and TP53 mutation status are also shown. Box plots as in Fig. 4. Source data