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. 2018 May 10;8:7477. doi: 10.1038/s41598-018-25544-z

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© The Author(s) 2018

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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Mutational signatures in RCC with VTT. (A) Mutational signature analysis of the five patients. The shown signatures represent the following mutational processes: AC1 = spontaneous deamination; AC2 = APOBEC action; AC3 = homologous recombination repair defect; AC5 = unknown/metabolic stress; AC9 = Pol eta/somatic hypermutation; AC13 = APOBEC; AC17 = unknown. Note the presence of AC3 indicating defective homologous recombination repair in three of the five patients (RCC-VTT-01, -04, -05). (B) Scatterplot of exposures to signature AC3 and indel counts (2–10 bp) per sample. Wilcoxon rank-sum test between the two colour-coded groups, p ≤ 0.0001.