PT - JOURNAL ARTICLE AU - A O-O Chan AU - S-K Lam AU - B C-Y Wong AU - W-M Wong AU - M-F Yuen AU - Y-H Yeung AU - W-M Hui AU - A Rashid AU - Y-L Kwong TI - Promoter methylation of <em>E-cadherin</em> gene in gastric mucosa associated with <em>Helicobacter pylori</em> infection and in gastric cancer AID - 10.1136/gut.52.4.502 DP - 2003 Apr 01 TA - Gut PG - 502--506 VI - 52 IP - 4 4099 - http://gut.bmj.com/content/52/4/502.short 4100 - http://gut.bmj.com/content/52/4/502.full SO - Gut2003 Apr 01; 52 AB - Background:E-cadherin is an adhesion molecule involved in tumour invasion/metastasis. Silencing of E-cadherin by promoter CpG methylation has been shown in both familial and sporadic gastric cancers. Helicobacter pylori is a class I carcinogen in gastric cancer. Aims: This study was undertaken to investigate the association between methylation of E-cadherin and H pylori in gastric mucosa from dyspeptic patients, and in intestinal metaplasia and primary and metastatic adenocarcinoma from surgical specimens of patients with gastric cancer. Methods:E-cadherin methylation was studied using methylation specific polymerase chain reaction in microdissected tissue from biopsies or surgical resection specimens. E-cadherin expression was studied by immunohistochemistry. Results:E-cadherin methylation was present in 31% (11/35) of gastric mucosae from dyspeptic patients, and was associated with H pylori infection (p=0.002), but was independent of the age of the patient or presence or absence of gastritis. E-cadherin methylation was present in 0% (0/8) of normal mucosa, 57% (12/21) of intestinal metaplasias, and 58% (15/26) of primary and 65% (21/32) of metastatic cancers. E-cadherin methylation status was concordant in 92% (11/12) of intestinal metaplasias and primary cancers, and in 85% (17/20) of primary and metastatic cancers from the same resected specimen. E-cadherin methylation in gastric cancer was associated with depth of tumour invasion (p=0.02) and regional nodal metastasis (p=0.05). Conclusion:E-cadherin methylation is an early event in gastric carcinogenesis, and is initiated by H pylori infection.