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. 2020 Jul 3;5:27. doi: 10.1038/s41525-020-0134-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a A Venn diagram of SNVs shows 0.49% overlap between tumours. b Variant Allele Frequencies (VAFs) of putative driver mutations show heterogeneous drivers in A1 and A2. c Mutational signature analysis. d Genomic landscape of CNAs shows CIN in both A1 (ploidy of 3.58) and A2 (ploidy of 2.2). e Log-ratio of putative driver CNAs highlights heterogeneity of tumourigenic events between A1 and A2. f Microbial analysis of DNA data shows microbial abundance at the phylum level. g Quantification of tumour immune infiltration for eight immune cell populations across A1 and A2.