Figure 3
Figure 3. Independent events involving the TP53 locus. Copy number profiles and mutation data were derived from high-resolution copy number arrays and whole-exome sequencing data, respectively. The clonal evolution in one patient from presentation to relapse as predicted by PhyloWGS19 and as further interpreted after inclusion of copy number data are shown in (A). The cancer clonal fractions of mutations detected in this patient are presented in (B). Mutations were manually assigned to clusters/subclones. In both plots, blue denotes aberrations/clones detectable only at presentation, red indicates aberrations/clones found only at relapse, and aberrations/clones present at both time points are shown in purple. Mutations in (B) that were not assigned to a cluster are depicted in gray. The LogR ratio for chromosome 17 at presentation and relapse is shown in (C). The major clone at presentation contained a NRAS mutation and a deletion at 17p involving the TP53 locus. This clone declined, whereas a new clone appeared with a KRAS and a TP53 mutation at relapse.

Independent events involving the TP53 locus. Copy number profiles and mutation data were derived from high-resolution copy number arrays and whole-exome sequencing data, respectively. The clonal evolution in one patient from presentation to relapse as predicted by PhyloWGS19  and as further interpreted after inclusion of copy number data are shown in (A). The cancer clonal fractions of mutations detected in this patient are presented in (B). Mutations were manually assigned to clusters/subclones. In both plots, blue denotes aberrations/clones detectable only at presentation, red indicates aberrations/clones found only at relapse, and aberrations/clones present at both time points are shown in purple. Mutations in (B) that were not assigned to a cluster are depicted in gray. The LogR ratio for chromosome 17 at presentation and relapse is shown in (C). The major clone at presentation contained a NRAS mutation and a deletion at 17p involving the TP53 locus. This clone declined, whereas a new clone appeared with a KRAS and a TP53 mutation at relapse.

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