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Fig. 2 | Clinical Epigenetics

Fig. 2

From: DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways

Fig. 2

TET1 and TET2 are suppressed in SSA and CIMP-CC carrying BRAFV600E. aTET1, TET2, and hMLH1 mRNA expression, presented as relative expression compared to paired normal mucosa. P values were calculated with Welch two sample t-test and error bars denote SD. b IHC of TET1 and TET2 in healthy normal mucosa (HNM) and cancers with wild type BRAF and KRAS (BRAFWT/KRASWT), mutated BRAF (BRAFV600E/KRASWT) or KRAS (BRAFWT/KRASG12/13). Representative example for each category (left) with quantitation (right) showing in red mean (circle) and median (line). P values were calculated with Wilcoxon rank-sum test. c β-values at TET1 and TET2 measured by HM27K. P values were calculated with Wilcoxon rank-sum test. d DNA methylation at TET1, TET2, and hMLH1 promoter-CGIs by bisulfite-pyrosequencing in samples from panel a. Schematic shows 6 sequencing regions (R1–R6) within TET1 (nt − 16 to + 800), 3 sequencing regions (R1–R3) within TET2 (nt − 140 to + 566) and 3 sequencing regions (R1–R3) with in distal promoter of hMLH1 (nt − 1080 to + 200) with primer positions (arrows), CpGs (black vertical lines), CpGs not analyzed (grey vertical lines), transcription start sites (TSS, red). Scatter plots of mean methylation levels for each CpG (left) and boxplots of the resultant methylation levels (right). P values were calculated with Wilcoxon rank-sum test. TA tubular adenoma, SSA/P sessile serrated adenoma/polyp

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