Figure 2: Epigenetic signatures correspond to cancer progression.
From: Semiconductor-based DNA sequencing of histone modification states
(a) A comparison of accumulated H3K4me3 profiles in a pair of matching metastasis and primary tumour cell lines. Shown are the number of ChIP-seq reads over 1 kb upstream and 1 kb downstream of transcription start site of each of 20,000 human genes in a matched pair of primary melanoma tumour (WM115, black, x axis) and metastasis (WM266-4, blue, y axis) cell lines derived from the same patient. The Pearson correlation coefficient is in the bottom right corner. (b,c) Density profiles of normalized reads from H3K4me3 ChIP-seq of primary melanoma tumour-derived cell line (WM115) or metastasis-derived cell line (WM266-4) at illustrative loci with either lower (b) or higher (c) levels of H3K4me3 in the metastasis-derived cell line. (d–g) Gene sets enriched (by GSEA) among loci with different levels of histone modifications. In each case, shown are the names of the enriched gene sets (rows) along with the normalized enrichment score, enrichment P-value and false discovery rates. Each entry in the heat map indicates the percent overlap in ‘leading edge genes’ (those that contribute to the enrichment) between two enriched gene sets. (d) Genes with lower H3K4me3 in metastasis cell line (WM266-4) relative to control primary tumour cell line (WM115). (e) Genes with higher H3K4me3 in metastasis cell line (WM266-4) relative to control primary tumour (WM115). (f) Genes with lower H3K4me3 in metastatic melanoma tumours from patients (an average of seven tumours samples) relative to control normal skin melanocytes (an average of three biological samples). (g) Genes with higher H3K4me3 in metastatic melanoma tumours from patients relative to control normal skin melanocytes.
