Skip to main content
Fig. 1 | Genome Biology

Fig. 1

From: A systematic dissection of the epigenomic heterogeneity of lung adenocarcinoma reveals two different subclasses with distinct prognosis and core regulatory networks

Fig. 1

Distinct H3K27ac profiles in LUAD and normal lung tissues. a Unsupervised hierarchical clustering of H3K27ac profiles for tumor and normal lung tissues of LUAD patients based on pairwise Pearson correlation coefficients (PCCs). b An MA plot of differential H3K27ac-modified sites between tumor and normal tissues, “M” represented log 2 fold change and “A” represented average log 2 signal intensities, sites with |M value| ≥ 1 and adjust p-value ≤ 0.05 defined as differential sites. c A heatmap of the H3K27ac signal in differential sites identified in b. The H3K27ac signal is represented as row-normalized z-scores. d Differential H3K27ac enrichment in super-enhancers (SE) between tumor and normal tissues. Each row represents an SE with a different enrichment between two tissues. SE scores are represented as row-normalized z-scores. Important differential SE-associated genes shown in the right. e Ranked plot for tumor-specific SE-associated TFs. IHC staining validated TFs are indicated with lines. f IHC staining results of 4 tumor samples showed tumor-specific SE-associated SOX9 were highly expressed in tumor. g The functional enrichment of tumor-specific (left) and normal-specific (right) SE-associated genes. h Track plots of the H3K27ac signal distribution in tumor (top) and normal (bottom) samples across the SOX9 (tumor-specific super-enhancer associated genes), CAV1-CAV2 (normal-specific super-enhancer associated genes), and MET (other super-enhancer associated genes) loci. “SOX9-SE” represented this super-enhancer associated with SOX9. “CAV2&CAV1-SE” represented this super-enhancer associated with CAV2 and CAV1. “MET-SE” represented this super-enhancer associated with MET. Heatmap of log2 fold change indicates the H3K27ac signal differences between tumor and normal tissues. i An example of super-enhancer hijacking. Number of junction reads from RNA-seq supported EML4 and ALK gene fusion showed in the top left panel. Model of super-enhancer hijacking through chromosome translocation showed in the top right panel. Track plots of the H3K27ac signal distribution and gene expression in fusion and non-fusion samples across the EML4 and ALK loci (bottom)

Back to article page