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. 2019 May 20;14:45. doi: 10.1186/s13000-019-0826-0

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — Representative results of fluorescence in situ hybridization (FISH) analysis and Sanger sequencing of primary CNS A-DLBCL. The FISH analysis for patient 1 showed extra copy signals for BCL6 (a), BCL2 (b) and MYC (c). MYD88 L265P mutations in patients 1 (d) and 2 (e), in which a CTG (leucine) codon was changed to a CCG (proline) codon. TP53 R273C mutation of patient 3 (f), in which a CGT (arginine) codon was changed to a TGT (cysteine) codon