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. 2018 Dec 7;9:5235. doi: 10.1038/s41467-018-07552-9

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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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Fig. 2 — Viral and non-viral mechanisms of CCNE1 activation in HCC. a Summary of structural rearrangements (top) and viral insertions (bottom) affecting CCNE1 gene identified in 751 HCC from the LICA-FR, TCGA and ICGC-JP cohorts. b Sorted CCNE1 expression (log scale) in the LICA-FR and TCGA cohorts. Gene expression was obtained from RNA-seq data and is given in fragments per kilobase of exons per million reads (FPKM). Samples harboring structural variants (SV), focal amplifications and viral insertions are indicated with a color code. c Functional consequences of structural rearrangements affecting CCNE1 regulatory region. RNA-seq read counts along CCNE1 locus are represented in normal liver (top) and in 4 tumors harboring structural rearrangements upstream CCNE1 trancription start site (TSS). H3K27Ac chromatin immunoprecipitation sequencing (ChIP-seq) signal and chromatin states in adult liver were obtained from the ROADMAP consortium and are depicted below each reconstruted DNA sequence. EnhA: active enhancer; EngG: genic enhancer; EnhWk: weak enhancer; TssA: active TSS; TssFlnk: flanking TSS; TxWk: weak transcription; Quies: quiescent chromatin