Additional file 1 of Cancer-specific CTCF binding facilitates oncogenic transcriptional dysregulation

Additional file 1: Fig. S1. Identification of cancer-specific CTCF binding sites. Fig. S2. Characterization of cancer-specific lost/gained CTCF binding sites. Fig. S3. Cancer-specific lost/gained CTCF binding sites associate with changed chromatin accessibility in patients. Fig. S4. Cancer-specific lost/gained CTCF binding sites associate with changed local chromatin interactions in different scales. Fig. S5. Lost/gained CTCF binding events associate with chromatin dynamics regardless of CTCF motif. Fig. S6. Histone modification patterns at cancer-specific lost and gained CTCF binding sites. Fig. S7. Histone modification patterns in normal CD4+ T-cell, T-ALL cell lines and T-ALL patients at T-ALLlost and T-ALLgained CTCF binding sites. Fig. S8. Cancer-specific loss/gain of CTCF events correlate with gene expression. Fig. S9. Patterns of differential DNA methylation near cancer-specific lost and gained CTCF sites with and without CTCF motif. Fig. S10. CTCF binding loss/gain events in T-ALL cell lines and T-ALL patients do not associate with DNA sequence mutations. Fig. S11. CTCF binding loss/gain events in 5 cancer types do not associate with DNA sequence mutations observed in ICGC samples. Fig. S12. Mutation rates around lost/gained CTCF binding sites in 6 cancer types. Fig. S13. Sequence motif analysis on cancer-specific lost and gained CTCF binding sites. Fig. S14. Cancer-specific gained CTCF correlate with oncogenic transcription factor. Fig. S15. Hi-C interaction maps in T-ALL cell line Jurkat and CD4+ T-cell. Fig. S16. Cancer-specific gained CTCF binding sites correlate with oncogenic transcriptional activation. Fig. S17. Pathway and Gene Ontology analyses of the genes located in the same chromatin domain with gained/lost CTCF sites for each cancer.