Skip Navigation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (13)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Graziano, F.
Right arrow Articles by Cascinu, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Graziano, F.
Right arrow Articles by Cascinu, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Annals of Oncology 15:489-492, 2004
© 2004 European Society for Medical Oncology


Original Paper

Combined analysis of E-cadherin gene (CDH1) promoter hypermethylation and E-cadherin protein expression in patients with gastric cancer: implications for treatment with demethylating drugs

Received 19 August 2003; accepted 19 December 2003

Background:

Hypermethylation is studied as a new, relevant mechanism for silencing tumor suppressor genes. It is a potentially reversible epigenetic change and it is the target of novel anticancer compounds with demethylating activity. In this perspective, we investigated E-cadherin gene (CDH1) promoter hypermethylation in gastric carcinomas and its correlation with E-cadherin protein expression.

Methods:

Consecutive cases of gastric carcinoma with assessable paraffin-embedded tumor blocks and paired normal mucosa were considered eligible for study entry. CDH1 promoter hypermethylation and E-cadherin protein expression were determined by methylation-specific polymerase chain reaction and immunohistochemistry, respectively.

Results:

CDH1 promoter hypermethylation was found in 20 out of 70 gastric carcinomas and the epigenetic change occurred in the early, as well as in the locally advanced disease. In five cases, hypermethylation was also detected in the normal mucosa. Eighteen out of 20 hypermethylated tumors were of the diffuse histotype (P = 0.0001). Of 24 tumors with reduced or negative E-cadherin expression, 19 were hypermethylated and 5 were unmethylated (P = 0.0001).

Conclusions:

CDH1 promoter hypermethylation frequently occurs in gastric carcinomas of the diffuse histotype and it is significantly associated with downregulated E-cadherin expression. The knowledge on the hypermethylation status of tumor suppressor genes may be relevant to the development of demethylating drugs and novel chemopreventive strategies in solid tumors.

F. Graziano1,*, F. Arduini2, A. Ruzzo3, A. Mandolesi2, I. Bearzi2, R. Silva4, P. Muretto5, E. Testa1, D. Mari4, M. Magnani3, M. Scartozzi6 and S. Cascinu6

1 Medical Oncology Unit, Hospital of Urbino; 2 Department of Histopathology, University of Ancona; 3 Institute of Biochemistry ‘G Fornaini’, University of Urbino; 4 Medical Oncology Unit, Hospital of Fabriano; 5 Department of Histopathology, Hospital of Pesaro; 6 Medical Oncology, University of Ancona, Italy

Key words: gastric neoplasms, gastric carcinoma, E-cadherin, methylation, tumor suppressor gene


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Ann OncolHome page
P. Muretto, A. Ruzzo, F. Pizzagalli, F. Graziano, P. Maltese, C. Zingaretti, E. Berselli, N. Donnarumma, and M. Magnani
Endogastric capsule for E-cadherin gene (CDH1) promoter hypermethylation assessment in DNA from gastric juice of diffuse gastric cancer patients
Ann. Onc., March 1, 2008; 19(3): 516 - 519.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.