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Promoter methylation of E-cadherin gene in gastric mucosa associated with Helicobacter pylori infection and in gastric cancer
  1. A O-O Chan1,
  2. S-K Lam1,
  3. B C-Y Wong1,
  4. W-M Wong1,
  5. M-F Yuen1,
  6. Y-H Yeung1,
  7. W-M Hui1,
  8. A Rashid2,
  9. Y-L Kwong1
  1. 1Department of Medicine, Queen Mary Hospital, Hong Kong
  2. 2Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
  1. Correspondence to:
    Dr Y L Kwong, University Department of Medicine, Professorial Block, Queen Mary Hospital, Pokfulam Road, Hong Kong;
    ylkwong{at}hkucc.hku.hk

Abstract

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.

  • E-cadherin methylation
  • gastric cancer
  • intestinal metaplasia
  • Helicobacter pylori
  • PCR, polymerase chain reaction
  • MSP, methylation specific polymerase chain reaction
  • COX-2, cyclooxygenase 2

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