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Promoter methylation of p16 associated with Helicobacter pylori infection in precancerous gastric lesions: A population‐based study
Author(s) -
Dong CaiXuan,
Deng DaJun,
Pan KaiFeng,
Zhang Lian,
Zhang Yang,
Zhou Jing,
You WeiCheng
Publication year - 2008
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.23891
Subject(s) - helicobacter pylori , gastroenterology , intestinal metaplasia , medicine , dysplasia , odds ratio , methylation , gastritis , cancer , atrophic gastritis , gastric mucosa , biopsy , population , stomach , biology , biochemistry , environmental health , gene
To investigate the relationship between p16 methylation and Helicobacter pylori infection in precancerous gastric lesions, a population‐based study was conducted in Linqu County, a high‐risk area of gastric cancer in China. Methylation status of p16 was evaluated by methylation‐specific polymerase chain reaction in 920 subjects with precancerous gastric lesions. H. pylori status was determined by 13 C‐urea breath test and the density of H. pylori in biopsy specimens used for detecting methylation status was assessed by the modified Giemsa stain. The frequency of p16 methylation was significantly higher in subjects with H. pylori positive than those with H. pylori negative in each category of gastric lesion ( p < 0.001, respectively). Compared with H. pylori negative, the odds ratios (ORs) of p16 methylation were markedly elevated in subjects with H. pylori positive for superficial gastritis (OR, 9.45; 95% confidence interval [CI]: 2.94–30.41), chronic atrophic gastritis (OR, 15.92; 95%CI: 7.60–33.36), intestinal metaplasia (OR, 4.46; 95%CI: 2.44–8.13), indefinite dysplasia (OR, 3.67; 95%CI: 1.90–7.10), and dysplasia (OR, 2.48; 95%CI: 1.02–5.99). Moreover, the frequencies of p16 methylation increased steadily with the severity of H. pylori density in gastric mucosa. Compared with H. pylori negative, the OR of p16 methylation was 1.02–16.13 times higher in subjects with mild H. pylori infection, and 2.69–38.73 times higher in those with moderate/severe infection, respectively. Our findings indicate that p16 methylation was significantly associated with H. pylori infection in precancerous gastric lesions, suggesting that H. pylori infection could potently induce methylation of p16 CpG island. © 2008 Wiley‐Liss, Inc.