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. 2020 Nov 5;10:19189. doi: 10.1038/s41598-020-76206-y

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Mouse tumor exome sequencing in IL-6^+/-/Pax5^+/- B-ALL. (a) Whole-exome sequencing analysis of tumor and control samples. Tumor-specific somatic mutations were determined by mutect and varscan analysis. The number of somatic cancer genes was calculated by using the cancer gene consensus list. The percentage of leukemic cells for each mouse was: 98% (U971) from total BM, 90% (U572) from total BM, 90% (L370) from total BM and 20% (L371) from total LN. (b) Genomic comparison between mutations driving native B-ALL as a result of natural infection exposure of IL-6^+/+/Pax5^+/- (previously described in Martin-Lorenzo, A. et al.⁹) (orange) and IL-6^+/-/Pax5^+/- mice (violet), respectively, showed that similar second hits were affected by recurrent mutations.