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. 2018 Jan 18;8:1032. doi: 10.1038/s41598-018-19389-9

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© The Author(s) 2018

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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Identification of MN1:BEND2 fusion. (A) Cartoon of fusion between exon 1 of MN1 (22q12.1, orange) and exons 9–14 of BEND2 (Xp22.13, blue), with spanning reads from RNAseq from sample (F) underneath. (B) Top: RT-PCR using primers designed against MN1, BEND2, and spanning the breakpoint, in samples (E), (F) and (H). KNS42 paediatric glioblastoma cells were used as a fusion-negative control. Beta actin (ACTB) was used as a positive RT-PCR control. Bottom: Sanger sequencing of the fusion band in sample. (E) Showing a sequence spanning the breakpoint. (C) FISH using probes directed against MN1 (green) and BEND2 (red), detecting fusion signals throughout sample (H). (D) RNAseq coverage of BEND2, with high levels of expression of exons 9–14 in sample (E).