Fig. 1: TP53 mutation in Oesophageal Squamous Cell Carcinoma (ESCC).

a 88 TCGA ESCC samples were analyzed to identify the prevalence of genome alterations (single nucleotide variants, SNV, loss of heterozygosity, LOH & copy number variation, CNV) in the TP53 gene. 74% of samples reported LOH over TP53 and 84% reported SNVs. 64% of samples reported both SNVs and LOH over TP53. See Supplementary Data 1 for source data. b Cell behaviour in basal layer of normal homoeostatic epithelium. On division, a progenitor may generate two dividing progenitors, two differentiating daughters, or one cell of each type. r is the probability of symmetric division outcome. On average, equal proportions of progenitor and differentiating cells are generated. c, d TP53 mutant clones in normal human oesophagus, data from ref. 2. c Protocol: normal oesophageal epithelium was cut into a contiguous grid of 2 mm² samples and ultradeep targeted sequencing of 74 cancer genes, including TP53, performed. SNV were called and those spanning adjacent samples merged to generate the variant allele frequency (VAF) for each SNV. d VAF of TP53 mutants. VAFs of missense mutants at codons 175, 245, 248, 249 273, and 282 are compared with the other missense (other ms) and nonsense and essential splice mutants (ns/splice). n = 16, 12, 20, 5, 23, 17, 307, and 101 clones respectively. Boxes indicate quartiles, horizontal bar median and whiskers indicate range, up to 1.5 fold inter-quartile range. p values, Kruskal–Wallis test for between group differences with Dunnett’s correction for multiple comparisons. See Supplementary Data 2.