DNA methylation of distal regulatory sites characterizes dysregulation of cancer genes
1 The Department of Developmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Faculty of Medicine, Hebrew University-Hadassah Medical School, Ein Kerem Campus, Jerusalem 91120, Israel
2 The Rachel and Selim Benin School of Computer Science and Engineering, Hebrew University of Jerusalem, Edmond J. Safra Campus, Jerusalem 91904, Israel
Genome Biology 2013, 14:R21 doi:10.1186/gb-2013-14-3-r21Published: 12 March 2013
Additional file 1:
Supplementary tables and figures. Table S1. Human cell types and DNA methylation data that used in the development of the promoter-based model. Table S2.Normal and cancer cell types used in the study. Table S3. Genes that are hypomethylated and upregulated in the examined cancer types, compared with normal cells.Table S4. Enriched GO groups among the genes that were hypomethylated and upregulated in various cancers.Table S5.Hypomethylatedupregulatedgenes in acute leukemia.Figure S1.The overall structure of the DNA methylation data. Figure S2. Methylation levels around TSSs as function of gene expression levels.Figure S3.Genomic sites are hypomethylated when marked as enhancer chromatin, compared with the methylation of the same sites in non-regulatory chromatin.Figure S4.An example of a long-range enhancer-promoter interaction captured by both methylation-based gene-enhancer pairing and long-range chromatin interactions assessed by the 5C technique.Figure S5.Representative examples of methylation-based gene-enhancer pairing.
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Additional file 2:
Data file. A CSV file (3.3 MB) denoting CpG position and gene symbols for the 118,417 CpG-gene pairs that obtained score >0.75.
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