Helicobacter pylori infection in relation to E-cadherin gene promoter polymorphism and hypermethylation in sporadic gastric carcinomas

Figure 1 Immunohistochemical staining. A: Positive (++) immunohistochemical staining for E-cad expression in non-cancerous epithelium; B: Negative (-) immunohistochemical staining for E-cad expression in cancerous lesion in diffuse type tumor.

Figure 2 RFLP analysis of genetic polymorphism of the 160 site of the E-cad promoter. The C/A polymorphism was differentiated by BstEII digestion of PCR products homozygous for the wild-type (high-activity) allele (wt/wt, CC genotype), heterozygous for the variant (low-activity) allele (wt/vt, CA genotype), and homozygous for the low-activity allele (vt/vt, AA genotype).

Figure 3 Gel electrophoresis picture demonstrating aberrant methylation in E-cad. Primer sets used for simple amplification are designed as unmethylated (U), methylated (M), unmodified DNA (N). Water is used as a negative control (H2O). Molecular weight marker is 100-bp DNA ladder. A: Methylation in non-cancerous epithelium. Samples 51, 57, and 60 N are methylated. Sample 59 N is unmethylated; B: Methylation in cancerous lesion. Samples 3, 8, and 34 T are methylated. Samples 26 and 28 T are unmethylated.