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

doi:10.3748/wjg.v11.i33.5174

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Helicobacter Pylori

World J Gastroenterol. Sep 7, 2005; 11(33): 5174-5179
Published online Sep 7, 2005. doi: 10.3748/wjg.v11.i33.5174

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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).

Citation: Liu YC, Shen CY, Wu HS, Chan DC, Chen CJ, Yu JC, Yu CP, Harn HJ, Shyu RY, Shih YL, Hsieh CB, Hsu HM. Helicobacter pylori infection in relation to E-cadherin gene promoter polymorphism and hypermethylation in sporadic gastric carcinomas. World J Gastroenterol 2005; 11(33): 5174-5179
URL: https://www.wjgnet.com/1007-9327/full/v11/i33/5174.htm
DOI: https://dx.doi.org/10.3748/wjg.v11.i33.5174