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. 2018 May 16;8:7735. doi: 10.1038/s41598-018-25462-0

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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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(a) Distribution of V_R:D in somatic mutations between CGC and non-CGC genes. (b) Distribution of V_R:D in somatic mutations categorized based on their predicted effect on the protein function in the entire dataset and in the CGC subset. (c) The mutation categories correspond to: generating a premature termination codon variant (PTV), substitution of an amino acid (missense) or not altering a coding sequence (silent). In both analyses the PTVs presented with significantly different distribution of V_R:D (p < 0.05) expressed as lower average allele fraction and a higher proportion of SOM-L mutations (V_R:D ~ 0). However, while still significantly different, the PTV V_R:D in the CGC genes appears more similar to the V_R:D of missense and silent variants, as compared to the pooled data from all genes. (d) Distribution of V_R:D in PTV, missense and silent variants in individual cancer types across the entire dataset, and (e) in CGC-genes.