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. 2021 Jun 1;22:167. doi: 10.1186/s13059-021-02375-2

Fig. 3.

Fig. 3

CBS epimutation associates with CIMP in multiple tumors and in gastric intestinal metaplasia. a Box plot showing CBS gene expression levels in CIMP, non-CIMP, and normal categories per cancer type (CIMP vs non-CIMP; *P < 0.05, two-sided Wilcoxon rank sum test). b Box plot showing mean promoter methylation β-values of CBS gene in CIMP, non-CIMP, and normal categories per cancer type (CIMP vs non-CIMP; *P < 0.05, two-sided Wilcoxon rank sum test). c Breakdown of GIM CIMP [upper panel] and GC CIMP [lower panel] signatures in CpG contexts island, shore, shelf, and open sea; *P < 0.001 according to binomial test; “Annotated” refers to the distribution of CpG probes on the Infinium methylation array. d Three-way Venn overlap of hypermethylated or hypomethylated CpG sites in GIM CIMP and GC CIMP subtypes at CGI level. e Average promoter methylation β-values of CBS gene in normal [chronic gastritis] and antrum GIM lesions based on CIMP (high), and non-CIMP (intermediate) (*P < 0.05 in pair-wise two-tailed Mann-Whitney test with mean β-value difference ≥ 0.2 compared to normal group). f Average promoter methylation β-values of CBS gene in GIM cases with or without regression at study-end point; cases in pink belong to CIMP subtype (*P < 0.05 in pair-wise two-tailed Mann-Whitney test)