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. 2020 Jun 19;10(6):70. doi: 10.1038/s41408-020-0336-z

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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. 2 — a The median burden of nonsynonymous mutations increases with disease stage. pPCL (median 99, range 74–468), MGUS (median 20, range 1–66), and MM (median 64, range 11–2263), ***p < 0.001. b The prevalence of the APOBEC signature in the pPCL cohort. Only three patients (13% of total group and 33% of patients with MAF translocations) had a high percentage of the APOBEC signature, which is lower than reported in non-pPCL MM. c The amount of nonsynonymous mutations per cytogenetic subgroup is shown in (a). The median number of nonsynonymous mutations is relatively high in each subgroup: t(11;14) (median = 84, mean = 84), hyperdiploidy (HRD) (median = 104, mean = 100) and MAF including t(14;16) and t(14;20) (median = 112, mean = 171). There was no statistical significant difference between these groups. d The mutational load within the maf-subgroup between patients with a high APOBEC contribution compared to those with a not substantially increased APOBEC contribution.