Promoter methylation of p16 associated with Helicobacter pylori infection in precancerous gastric lesions: A population-based study
Promoter methylation of p16 associated with Helicobacter pylori infection in precancerous gastric lesions: A population-based study
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p16 启动子甲基化与癌前病变幽门螺杆菌感染相关：一项基于人群的研究
DOI：
10.1002/ijc.23891
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发表时间：
2009-01-15
影响因子：
6.4
通讯作者：
You, Wei-Cheng
中科院分区：
文献类型：
--
作者：
Dong, Cai-Xuan;Deng, Da-Jun;You, Wei-Cheng
为了探讨胃癌前病变中p16甲基化与幽门螺杆菌感染的关系，我们在中国胃癌高发地区临朐县开展了一项基于人群的研究。通过甲基化特异性聚合酶链反应对920例胃癌前病变患者的p16甲基化状态进行了评估。采用c -13-尿素呼气试验测定H. pylon状态，采用改良Giemsa染色法评估用于检测甲基化状态的活检标本中H. pylon的密度。幽门螺杆菌阳性受试者的p16甲基化频率显著高于幽门螺杆菌阴性受试者（p < 0.001）。与幽门螺杆菌阴性患者相比，幽门螺杆菌阳性患者的p16甲基化优势比（ORs）在以下情况下显著升高：浅表性胃炎（OR, 9.45； 95%可信区间[CI]: 2.94-30.41）、慢性萎缩性胃炎（OR, 15.92; 95%CI: 7.60-33.36）、肠化生（OR, 4.46; 95%CI: 2.44-8.13）、不确定型不典型增生（OR, 3.67; 95%CI: 1.90-7.10）和不典型增生（OR, 2.48; 95%CI: 1.02-5.99）。此外，p16甲基化频率随着胃粘膜幽门螺杆菌密度的严重程度而稳步增加。与幽门螺杆菌阴性者相比，轻度幽门螺杆菌感染组p16甲基化OR值高1.02 ~ 16.13倍，中、重度幽门螺杆菌感染组p16甲基化OR值高2.69 ~ 38.73倍。我们的研究结果表明，胃癌前病变中p16甲基化与幽门螺杆菌感染显著相关，提示幽门螺杆菌感染可有效诱导p16 CpG岛甲基化。(C) 2008 Wiley-Liss。公司。
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. pylon status was determined by C-13-urea breath test and the density of H. pylon 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. pylon positive than those with H. pylori negative in each category or gastric lesion (p < 0.001, respectively). Compared with H. pylori negative, the odds ratios (ORs) 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 or p16 methylation increased steadily with the severity of H. pylori density in gastric mucosa. Compared with H. pylon 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. (C) 2008 Wiley-Liss. Inc.