Fig. 2: Genomic and transcriptomic analyses for patient B.
From: Personalised mapping of tumour development in synchronous colorectal cancer patients
a Venn diagrams of SNVs for all lesions B1–B5 (left) and for MSI lesions B1–B4 (right) show low overlap between tumours. b Putative phylogenetic tree based on driver mutations. c VAFs of putative driver mutations. d Mutational signature analysis. e Transcript counts of the MLH1 detected by RNA-seq analysis. f Genomic landscape of CNAs shows low CIN for MSI samples B1 (ploidy: 2), B2 (ploidy: 1.95), B3 (ploidy: 2) and B4 (ploidy: 1.98), and higher CIN for MSS sample B5 (ploidy: 2.13). g Median log-ratio of putative driver CNAs highlights heterogeneity of tumourigenic events between all lesions. h Microbial analysis of DNA data shows microbial abundance at the phylum level. i Quantification of tumour immune infiltration reveals distinct profiles for eight immune cell populations across B1–B5.
