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. Author manuscript; available in PMC: 2016 Jul 7.
Published in final edited form as: Nature. 2016 Jan 13;529(7586):351–357. doi: 10.1038/nature16478

Figure 4. Genetic divergence of recurrent medulloblastoma is driven by clonal selection.

Figure 4

a, Copy-neutral LOH PTCH1−/− driver status reverts to wild type post-therapy in medulloblastoma-REC-12, with homozygous CDKN2A/B loss. b, The evolutionary progression of medulloblastoma-REC-12 is illustrated by (pink) PTCH1+/− lineage expansion, copy-neutral LOH, clonal eradication during treatment, and (blue) subsequent expansion of an ancestral clone with CDKN2A/B−/−. c, Phylogenetic relationships between primary (red) and recurrent (blue) tumours show that recurrences often represent a single rather than multiple primary tumour lineages (for example, medulloblastoma-REC-05/12 compared with medulloblastoma-REC-02). d, Ultra-deep sequencing shows post-treatment expansion of low-frequency or de novo primary clones (blue), and eradication/reduction of therapy-sensitive lineages (red). Inset box indicates number of mutations per cluster.