Extended Data Fig. 3: Evolution of genomic occupancy and Sox2 activation changes from normal to neoplastic organoids.
From: Reprogramming of the esophageal squamous carcinoma epigenome by SOX2 promotes ADAR1 dependence

a, Heatmaps of H3K27ac ChIP-seq signal ±2ākb around Sox2 peaks (identified in Fig. 2a) across different organoids. Two independent biological replicates were performed and shown for each organoid. b, H3K4me1 ChIP-seq signals ±2ākb around Sox2 peaks (identified in Fig. 2a) across different organoids. Two independent biological replicates were performed and shown for each organoid. c, The ratio of SOX2 positive correlated genes from TCGA ESCC in Sox2 up/down/unaffected genes in the comparison of SCPP vs Normal organoid models, **** pā<ā0.0001 calculated by two-sided fisher exact test for 2āĆā2 contingency table. d, Genes that are significantly positively correlated with SOX2 in TCGA ESSC samples as a āGene Setā with Gene Set Enrichment Analysis (GSEA) used to quantify expression differences of the gene set between SCPP and Normal organoids. (Two-sided FDR-adjusted q-value=0.106; nominal pā=ā0.106 calculated by the GSEA package) e, Genes that are significantly positively correlated with SOX2 in TCGA ESSC samples as a āGene Setā with GSEA is used to quantify expression differences of the gene set between SCPP and CPP organoids. (Two-sided FDR-adjusted q-value<0.0001; nominal pā<ā0.0001 calculated by the GSEA package).