MOESM9 of Global impact of somatic structural variation on the DNA methylome of human cancers

Additional file 9. Related to Fig. 5. SSV associations with translocated active in vivo-transcribed enhancers. For the enhancer-related analyses of Fig. 5b, the Andersson et al. tissue- or cell-specific enhancer subsets as applied to each TCGA or ICGC project are listed. Results include the subset of SSV breakpoint associations involving the translocation of an active, in vivo-transcribed enhancer within 0.5â Mb of the gene (where the unaltered gene had no enhancer within 1â Mb), for both the entire set of SSV breakpoint associations occurring 0-500â kb upstream of a gene and with breakpoint mate on the distal side from the gene (for cases with WGS), as well as for the subset of SSV breakpoint associations involving altered gene expression or CGI methylation.补充文件9。与图5相关：体细胞结构变异（SSV, Somatic Structural Variant）与易位的体内转录激活增强子的关联。针对图5b的增强子相关分析，本文列出了Andersson等针对每个癌症基因组图谱（TCGA, The Cancer Genome Atlas）或国际癌症基因组联盟（ICGC, International Cancer Genome Consortium）项目所采用的组织或细胞特异性增强子子集。分析结果涵盖两类SSV断点关联子集：其一为在发生于基因上游0–500 kb且断点另一端位于基因远端侧（适用于全基因组测序（WGS, Whole Genome Sequencing）样本）的全部SSV断点关联集合中，涉及“未发生改变的基因1 Mb范围内无增强子，且于该基因0.5 Mb范围内存在易位的活性体内转录增强子”的子集；其二为涉及基因表达改变或CpG岛（CGI, CpG Island）甲基化改变的SSV断点关联子集。