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. Author manuscript; available in PMC: 2016 Sep 23.
Published in final edited form as: Cell Syst. 2015 Sep 23;1(3):210–223. doi: 10.1016/j.cels.2015.08.015

Figure 3. Tracking tumor evolution and refining a model of clonal architecture.

Figure 3

A) Variant allele frequency (VAF) of key mutations, at diagnosis (day 0), during progression through treatment, and at relapse (day 505). The median depth of coverage obtained at each variant position for each timepoint is indicated at top. Samples for intermediate timepoints between day 0 and 505 were obtained from FFPE blocks and in some cases were heavily degraded, leading to lower yields and sequence depth for some timepoints. B) Model of clonal architecture and tumor evolution, inferred from the original ~30× sequencing data. C) Ultra-deep sequencing and validation revealed additional subclonal complexity. D) Incorporating the results of single-cell sequencing and intermediate timepoints allows for refinements to the model, including establishing an independent origin for the TP53-mutant clonal population. Numbers in legend refer to cluster assignments. The ‘Chemotherapy’ label includes induction chemotherapy (day 1), and four rounds of consolidation chemotherapy at days 47, 81, 116, and 151.