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. 2011 Jul 5;105(3):372–381. doi: 10.1038/bjc.2011.243

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Copyright © 2011 Cancer Research UK

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 https://creativecommons.org/licenses/by/4.0/.

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Proposed model for the synthetic lethality of ATR inhibition in cells with inactivated PARP or XRCC1. Endogenously generated DNA damage, largely in the form of single-strand breaks or base damage that is processed to single-strand breaks, are repaired by PARP and XRCC1 to promote cell survival. Unrepaired breaks accumulate in the absence of PARP or XRCC1 activity leading to stalled replication forks or replication-associated double-strand breaks (detected by γH2AX foci), which activate ATR to promotes repair by HR (detected by Rad51 foci) and cell survival. If ATR is inhibited by NU6027, the replication lesions remain unrepaired and the cell dies.