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. 2017 Aug 29;7:9711. doi: 10.1038/s41598-017-09859-x

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© The Author(s) 2017

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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Model depicting the repression of DPYD by p53 following thymidylate synthase (TS) inhibition, dTTP imbalance and DNA damage. P53 transcriptionally represses DPYD expression and negatively impacts the catabolism of pyrimidines following inhibition of TS. In extension, this results in an imbalance in the dTTP/dUTP ratio and a need to salvage cellular levels of dTTP to maintain uninterrupted DNA replication and repair. However, in the presence of 5-FU this might cause increased cell death due to reduced catabolism and increased incorporation of the 5-FU metabolites FdUTP and FUTP into DNA and RNA respectively.