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. 2018 Jun 1;9:2150. doi: 10.1038/s41467-018-04530-z

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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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Fig. 1 — FOS fusions in osteoblastoma. a Clustered break points in FOS. b Central Circos plot showing the clustering of break points in FOS-mutant samples. All structural variants involving chromosome 14 are shown, demonstrating the paucity of genomic rearrangements. Surrounding panels demonstrate normalised RNA-Seq read counts for each fusion partner. Horizontal line segments reflect mean sequencing counts. The arrow above shows the direction of transcription of the fusion. c Retroviral v-fos. d Schematic of FOS break points in benign bone and vascular tumours generating similarity with the murine retroviral transforming v-fos. Subscript numbers from left to right report the length of the transcript to the stop codon and the predicted cleavage and poly-adenylation site, respectively. e FOS immunohistochemistry demonstrating strong nuclear immunoreactivity in FOS-mutant osteoblastoma, PD13482 (centre with zoom inset), Haematoxylin and eosin (H&E) (left), and a clear breakapart of FISH probes surrounding the FOS locus (right)