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. 2021 Mar 11;12:1602. doi: 10.1038/s41467-021-21891-0

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© The Author(s) 2021

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. 3 — A A set of tumors sequenced by WGS was stratified by two parameters: the y-axis separates APOBEC− tumors (bottom) from APOBEC+ tumors (top), and the x-axis separates tumors with high A3B character (left) from those with high A3A character (right). Points are colored by tumor type (legend at right). B When tumors are colored by the fraction of APOBEC mutations occurring in TpC hairpins, it is clear that tumors enriched for TpC hairpin mutations (red) tend to be A3A-dominated APOBEC+ samples. C When tumors are colored by the fraction of APOBEC mutations occurring in VpC hairpins, the same pattern is evident: tumors with the highest levels of VpC hairpin mutations (magenta) tend to be A3A-dominated tumors. D TpC and VpC hairpin mutations are tightly associated: tumors enriched for one are enriched for both, suggesting that A3A is the joint cause of both. E Comparison of A3A and A3B activity on DNA oligos representing non-hairpin TpC sites and hairpin VpC sites. A3A activity is seen on all substrates, but A3B activity is not observed at VpC sites. Source data are provided as a Source Data file.