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©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
Helicobacter pylori infection in relation to E-cadherin gene promoter polymorphism and hypermethylation in sporadic gastric carcinomas
Yao-Chi Liu, Chen-Yang Shen, Hurng-Sheng Wu, De-Chuan Chan, Cheng-Jueng Chen, Jyh-Cherng Yu, Cheng-Ping Yu, Horng-Jyh Harn, Rong-Yaun Shyu, Yu-Lueng Shih, Chung-Bao Hsieh, Huan-Mieng Hsu
Yao-Chi Liu, De-Chuan Chan, Cheng-Jueng Chen, Jyh-Cherng Yu, Chung-Bao Hsieh, Huan-Mieng Hsu, Division of General Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China
Rong-Yaun Shyu, Yu-Lueng Shih, Division of Gastroenterology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China
Cheng-Ping Yu, Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China
Horng-Jyh Harn, Department of Pathology, Buddhist Tzu-Chi General Hospital, Hualien, Taiwan, China
Hurng-Sheng Wu, Department of Surgery, Show Chwan Memorial Hospital, Changhua, Taiwan, China
Chen-Yang Shen, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, China
Author contributions: All authors contributed equally to the work.
Supported by Clinical Research Fund of the Tri-Service General Hospital and CY Foundation for Advancement of Education, Science and Medicine, Taipei, Taiwan, China
Correspondence to: Dr. Yao-Chi Liu, Division of General Surgery, Tri-Service General Hospital, No. 325, Sec. 2, Cheng-Kung Road, Neihu 114, Taipei, Taiwan, China. dlyaochi@yahoo.com.tw
Telephone: +886-2-87927191 Fax: +886-2-87927372
Received: December 30, 2004
Revised: February 15, 2005
Accepted: February 18, 2005
Published online: September 7, 2005
AIM: To study Helicobacter pylori (H pylori) infection in relation to E-cadherin (E-cad) promoter polymorphism and hypermethylation in GCs.
METHODS: Specimens were taken from representative cancerous lesions and adjacent non-cancerous epithelia of 67 resected GCs. H pylori was detected by real-time PCR of the cagA gene from non-neoplastic epithelium. E-cad promoter polymorphism and hypermethylation were determined by restriction fragment length polymorphism analysis and methylation-specific PCR, respectively. Expression of E-cad protein was determined by immunohistochemistry.
RESULTS: H pylori was found in 57% of patients with GC. H pylori infection was more frequently found in tumors with the -160C/C genotype than those with the -160C/A and -160A/A genotypes (74% vs 47%, P = 0.02). H pylori infection was associated with E-cad methylation in non-neoplastic epithelium; however, no significant difference in H pylori was observed between methylated and unmethylated cancerous lesions.
CONCLUSION: Patients with the -160C/C genotype might require H pylori infection to promote the inactivation of CDH1, suggesting that H pylori infection might affect GC in an initial stage because polymorphism is germ line. Mechanism of hypermethylation of CDH1 promoter in GC is complex, and H pylori infection might affect it in an initial stage.
