Enroth et al. BMC Cancer 2011, 11:450 http://www.biomedcentral.com/1471-2407/11/450 Page 3 of 13 Figure 1 ChIP-chip signals. (A) Signal example from the TWIST1-gene (chr7) with data from patient 2. Left panel shows individual probes in replicates for all signals after analysis in TAS. Right panel shows normalized and averaged signal in terms of standard deviations (y-axis). Detected regions and location (HG18) of the TWIST1 gene is also marked out. (B) Footprints of normal and tumor K4/K27 signal in patient 1 around the TSS’s (left) of genes associated with enriched regions in each group separately and centred around genes associated with bivalent regions (right) in normal and tumor respectively. material. In some cases, e.g. patient 1 tumor H3K27me3/K4me3, the correlation was highest with patient 2 normal H3K27me3/K4me3 rather than the HT29 cancer cell line. This pattern is more evident when regarding enriched regions only and by counting overlapping enriched regions, a relatively high similarity between normal and tumor samples and between patients for both H3K4me3 (Figure 3) and H3K27me3 was noted (Table 1 and Additional file 2, Figure S6). Around 60% of the H3K4me3 and 35% of H3K27me3 regions in both patients are common between normal and tumor tissue. When annotated transcripts rather than individual regions were used these numbers rise to around 70% and 50% respectively. Considering H3K4me3 genes, HT29 targets showed large overlaps with both patients normal and tumor samples (Table 1- 2). The overlaps for the adenocarcinoma cell line SW480 [24] were quite poor (10-20%) both with tissue samples and HT29 (Table 2). We also noted that the number (around 1%, 80-431) of bivalent regions detected in promoters here is lower than the number detected in a previous study [25] on differentiated cells