[ Back to EurekAlert! ] Public release date: 12-Apr-2010
[ | E-mail Share Share ]

Contact: Lin Tian
wjg@wjgnet.com
86-105-908-0039
World Journal of Gastroenterology

Factors increasing the risk of atrophic gastritis and intestinal metaplasia

Atrophic gastritis and intestinal metaplasia are two important precursory lesions in the process of intestinal type gastric cancer. However, the precise mechanism of the progression of these two lesions is still unclear, a few studies have investigated the risk of host gene polymorphism on the atrophic gastritis and intestinal metaplasia, but all of them are limited by their one-time point screen.

A research article to be published on April 14, 2010 in the World Journal of Gastroenterology addresses this question. The research team led by Professor Ji-You Li from Beijing cancer hospital & institute, Peking University used PCR based DHPLC technique and 56 month follow-up data, to study the association between IL-8, MIF gene polymorphisms and progression of atrophic gastritis and intestinal metaplasia in a high risk population of gastric cancer. The article further investigate the relationship of Helicobacter pylori infection and gene polymorphism on the progression of atrophic gastritis and intestinal metaplasia.

The result shown that IL-8-251 AA genotype or IL-8-251 AA genotype together with IL-8-251 TA genotype significantly increased the risk of severe atrophic gastritis and intestinal metaplasia; MIF-173 CC genotype or MIF-173 CC genotype together with MIF-173 GC genotype also increased the risk of severe atrophic gastritis and intestinal metaplasia significantly. Interestingly, the risk of severe atrophic gastritis and intestinal metaplasia become more evident when Helicobacter pylori infection has been considered.

Due to the high prevalence of H. pylori infection, antibiotic resistance, and some potential drawbacks associated with H. pylori eradication therapy (eg. reflux esophagitis), this study may provide a reasonable basis for therapeutic decisions (eg. Helicobacter pylori eradication) at an early stage of precursory lesions of gastric cancer.

###

Reference: Li ZW, Wu Y, Sun Y, Liu LY, Tian MM, Feng GS, You WC, Li JY. Inflammatory cytokine gene polymorphisms increase the risk of atrophic gastritis and intestinal metaplasia. World J Gastroenterol 2010; 16(14): 1788-1794

http://www.wjgnet.com/1007-9327/full/v16/i14/1788.htm

Correspondence to: Ji-You Li, Professor, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Pathology, Peking University School of Oncology, Beijing Cancer Hospital & Institute, Beijing 100142, China. lijiyou@263.net Telephone: +86-10-88192450 Fax: +86-10-88192437

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H. pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2008 IF: 2.081. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.



[ Back to EurekAlert! ] [ | E-mail Share Share ]

 


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.