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. 2021 Sep 22;12:5574. doi: 10.1038/s41467-021-25904-w

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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 Prevalence of replication stress (RS) alterations grouped by the mechanism of increased RS: (i) alterations leading to loss of RB pathway regulation and premature G1- > S phase entry, and (ii) alterations associated with oncogene-induced replication stress. Tumors with at least one of these alterations were classified as RS-high; tumors with none of these alterations were classified as RS-low. b Progression-free survival among patients with RS-low tumors. c Progression-free survival among patients with RS-high-negative tumors. Unlike patients with RS-low tumors, there was no benefit of addition of berzosertib to gemcitabine among patients with RS-high tumors.