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. 2019 Sep 2;10:3925. doi: 10.1038/s41467-019-11760-2

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© The Author(s) 2019

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. 7 — Model. a Cells that accumulate replication stress-associated DSBs are at a higher risk of genomic destabilization of either CIN or MSI. Genomic destabilization is associated with induction of mutations, leading to clonal evolution of cells with defects in cellular defense systems. b CIN is caused when replication stress-associated DSBs are not repairable, whereas MSI arises in association with erroneous DSB repair by MMEJ. Hypermutation is also induced in MMR-deficient cells