Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma

P. G. Corn, E. I. Heath, R. Heitmiller, F. Fogt, A. A. Forastiere, J. G. Herman, T. T. Wu

Research output: Contribution to journalArticle

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Abstract

Purpose: E-cadherin, a Mr 120,000 transmembrane glycoprotein, mediates calcium-dependent intercellular adhesion that is essential for normal tissue homeostasis. Loss of E-cadherin occurs in a variety of epithelial tumors and is correlated with invasion and metastasis. In esophageal adenocarcinoma, reduction of E-cadherin expression has been demonstrated previously, but mutations of the gene (CDH1) are rare. Experimental Design: In this study, we used a nested PCR approach to examine the methylation status of the 5′ CpG island of E-cadherin in esophageal specimens obtained from individuals with and without a history of esophageal cancer. Results: In four individuals without esophageal cancer, E-cadherin was completely unmethylated in normal squamous cell-lined esophageal mucosa. In contrast, in patients with esophageal adenocarcinoma, E-cadherin was methylated in 26 of 31 (84%) tumor specimens. In the majority of cases, matched normal tissue (esophagus or stomach) from each patient was completely unmethylated. By immunostaining, methylated tumor samples demonstrated heterogeneously decreased membranous E-cadherin staining. Conclusions: These data suggest that epigenetic silencing via aberrant methylation of the E-cadherin promoter is a common cause of inactivation of this gene in esophageal adenocarcinoma.

Original languageEnglish (US)
Pages (from-to)2765-2769
Number of pages5
JournalClinical Cancer Research
Volume7
Issue number9
StatePublished - 2001
Externally publishedYes

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CpG Islands
Cadherins
Adenocarcinoma
Esophageal Neoplasms
Methylation
Neoplasms
Gene Silencing
Epigenomics
Esophagus
Stomach
Glycoproteins
Homeostasis
Research Design
Epithelial Cells
Staining and Labeling
Neoplasm Metastasis
Calcium
Polymerase Chain Reaction
Mutation

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Corn, P. G., Heath, E. I., Heitmiller, R., Fogt, F., Forastiere, A. A., Herman, J. G., & Wu, T. T. (2001). Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma. Clinical Cancer Research, 7(9), 2765-2769.

Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma. / Corn, P. G.; Heath, E. I.; Heitmiller, R.; Fogt, F.; Forastiere, A. A.; Herman, J. G.; Wu, T. T.

In: Clinical Cancer Research, Vol. 7, No. 9, 2001, p. 2765-2769.

Research output: Contribution to journalArticle

Corn, PG, Heath, EI, Heitmiller, R, Fogt, F, Forastiere, AA, Herman, JG & Wu, TT 2001, 'Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma', Clinical Cancer Research, vol. 7, no. 9, pp. 2765-2769.
Corn PG, Heath EI, Heitmiller R, Fogt F, Forastiere AA, Herman JG et al. Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma. Clinical Cancer Research. 2001;7(9):2765-2769.
Corn, P. G. ; Heath, E. I. ; Heitmiller, R. ; Fogt, F. ; Forastiere, A. A. ; Herman, J. G. ; Wu, T. T. / Frequent hypermethylation of the 5′ CpG island of E-cadherin in esophageal adenocarcinoma. In: Clinical Cancer Research. 2001 ; Vol. 7, No. 9. pp. 2765-2769.
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AU - Herman, J. G.

AU - Wu, T. T.

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