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. 2023 Jan 13;83(6):814–829. doi: 10.1158/0008-5472.CAN-22-1444

Figure 1.

Figure 1. KDM6A mutation alters chromatin accessibility in human bladder cancers. A, Whole-exome sequencing of bladder cancer surgical specimens (n = 16). Seven KDM6A-wt (blue) and 4 KDM6A-mut (red) cases were chosen for ATAC-seq analysis. B, UMAP analysis of Cleveland Clinic bladder cancer specimens (KDM6A-wt in blue and KDM6A-mut in red) and TCGA genitourinary cancer specimens based on ATAC-seq data. C, Enriched motifs in accessible chromatin peaks specific for KDM6A-wt (blue) and KDM6A-mut (red) cancers. D, Functional enrichment analysis of accessible chromatin peaks enriched in KDM6A-wt cancers.

KDM6A mutation alters chromatin accessibility in human bladder cancers. A, Whole-exome sequencing of bladder cancer surgical specimens (n = 16). Seven KDM6A-wt (blue) and four KDM6A-mut (red) cases were chosen for ATAC-seq analysis. B, UMAP analysis of Cleveland Clinic bladder cancer specimens (KDM6A-wt, blue; KDM6A-mut, red) and TCGA genitourinary cancer specimens based on ATAC-seq data. C, Enriched motifs in accessible chromatin peaks specific for KDM6A-wt (blue) and KDM6A-mut (red) cancers. D, Functional enrichment analysis of accessible chromatin peaks enriched in KDM6A-wt cancers.