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. 2019 Dec 13;34(5):1315–1328. doi: 10.1038/s41375-019-0677-4

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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. 8 — Beta particles emitted by ¹⁷⁷Lu cause DNA double strand breaks that are recognized by the ATM/ATR sensor proteins. In Burkitt’s lymphoma (BL) and mantle cell lymphoma (MCL) cells, this leads to CHK1 phosphorylation and activation and consequently to phosphorylation of WEE-1 and MYT-1. This subsequently induces CDK1 phosphorylation at Tyr15 and Thr14, and G2/M cell cycle arrest to allow DNA repair. Conversely in follicular lymphoma (FL) cells, phosphorylation of CDK1 at Thr161 by CDK7 promotes G2/M cell cycle progression. Unrepaired DNA lesions lead to apoptosis.