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Additional file 1: of Recurrent mutations at estrogen receptor binding sites alter chromatin topology and distal gene expression in breast cancer

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posted on 2018-11-07, 05:00 authored by Jiekun Yang, Xiaolong Wei, Turan Tufan, Cem Kuscu, Hayrunnisa Unlu, Saadia Farooq, Elif Demirtas, Bryce Paschal, Mazhar Adli
Figure S1. ERBS shared by more patients contain more mutations after controlling for ER binding intensity. Figure S2. Comparable levels of somatic mutation burden are observed at ERBS overlapping promoter, intronic, and intergenic regions. Figure S3. ERBS are protected from somatic insertions and deletions, and the protective effect is correlated with ER binding intensity. Figure S4. Somatic mutations enriched at ERBS show the APOBEC mutational signature. Figure S5. ERBS with more mutations make more frequent chromatin interactions independent of ER binding intensity. Figure S6. ERBS associated with poor/met outcome contain more somatic mutations. Figure S7. Amplification plots for WT and mutant MCF-7 clones based on the qPCR colony screening strategy depicted in Figure 4d. Figure S8. Somatic mutation reduces ZBTB7A binding. ChIP-qPCR analysis shows ZBTB7A enrichment at the mutation site in MCF-7 WT cells and a mutant clone. Figure S9. High expression of TMEM41B, IPO7 and WEE1 is associated with poor survival for breast cancer patients. Figure S10. Somatic mutation burden at ERBS is higher when blood instead of adjacent to tumor breast tissue is used as “normal” in the mutation calling process. (PDF 2338 kb)

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National Cancer Institute

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