Fig. 4From: A survey of tandem repeat instabilities and associated gene expression changes in 35 colorectal cancersGene promoters in most cancer pathways are significantly enriched for repeat instability. Box plots of the proportion of promoters in five different cancer-associated signaling pathways with a) unstable repeats in their promoters and b) orphan repeats in their promoters, for normal-normal genome pairs (left boxes, n = 595) and for tumor-matched normal genome pairs (right boxes, n = 35). The pathways are: MAPK (number of genes in the pathway, N = 113), mTOR (N = 44), p53 (N = 98), TGF beta (N = 29), and Wnt (N = 87). Thick horizontal lines in each box mark the median, edges of boxes correspond to the 25th and 75th percentiles, and whiskers cover 99.3 % of the data’s range. In panel a repeat instability is significantly different in tumor genomes for the MAPK, p53, and Wnt signaling pathways (WRS test, P = 0.03, P < 10−8, P < 10−5, respectively, after Bonferroni correction). In panel b repeat instability is significantly different in tumor genomes for the MAPK, mTOR, p53, and Wnt signaling pathways (WRS Test, P < 10−31, P < 10−24, P < 10−9, P < 10−18, respectively after Bonferroni, correction)Back to article page