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. 2023 Aug 30;37(11):2237–2249. doi: 10.1038/s41375-023-02013-9

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Mutation diagram (lolliplot) for ZNF217. 31/157 PMBCL samples (19.7%) harbored ZNF217 SNVs or indels. Hot-spot mutations, truncating mutations (blue) and splice mutations (red) were labeled with specification of the alteration, SNVs are visualized in yellow. Domain data was obtained from Nunez et al. [55] and https://www.uniprot.org/. b Distribution of mutation types and c CNA of n = 157 PMBCL patients. In case of >1 alteration, the most deleterious type was attributed to the patient. d Comparison of ZNF217 mutation prevalence in PMBCL, HL and DLBCL. Patient-level data of ZNF217 was extracted from our data set and previous studies in PMBCL [7, 15], HL [17–19], and DLBCL [56–58]. Merged data were compared by two-sided fisher’s exact test. 95% CI of OR was calculated by Baptista-Pike method. Individual prevalence of the mutated gene in the present study is indicated by the dashed line.