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髓过氧化物酶多态性与胃癌风险的关联。

Association of the myeloperoxidase polymorphism with the risk of gastric cancer.

作者信息

Hsu Ping-I, Jwo Jyh-Jen, Yang Chia-Lin, Hsu Ping-Ning, Yang Hsiao-Bai, Lai Kwok-Hung, Chen I-Shu, Chuah Seng-Kee, Wu Deng-Chyang, Chen Angela

机构信息

Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

出版信息

Anticancer Res. 2008 Mar-Apr;28(2B):1317-23.

Abstract

BACKGROUND

The myeloperoxidase in neutrophils manufactures many bactericidal oxidants. The aim of this study was to clarify the relations between the myeloperoxidase polymorphism and gastric cancer development.

PATIENTS AND METHODS

In a case control study of 157 consecutive gastric cancer patients and 192 controls, the myeloperoxidase -463G-->A polymorphism was genotyped. Additionally, gastric mucosal changes were examined according to the updated Sydney System.

RESULTS

The carriage of myeloperoxidase allele A, male gender, advanced age, high intake of salty food and Helicobacter pylori infection independently increased the risk of gastric cancer [95% confidence interval (CI): 1.5-5.0, 1.7-6.5, 2.6-8.6, 1.1-2.6 and 1.2-3.8, respectively]. H. pylori-infected individuals who were carriers of myeloperoxidase allele A had increased risks of both intestinal and diffuse types of gastric cancer with odds ratios of 7.9 (95% CI 2.6-23.5) and 8.6 (95% CI 2.0-36.7), respectively. In the H. pylori-infected individuals, allele A carriers displayed higher scores of bacterial density (p=0.02) and neutrophil infiltration (p=0.05) in the antrum and higher scores of neutrophil infiltration (p=0.02) and gland atrophy (p=0.03) in the corpus than did non-carriers.

CONCLUSION

This study verifies the association of myeloperoxidase -463G-->A polymorphism with gastric cancer. The mechanisms underlying this genetic polymorphism in developing gastric cancer merit further investigations.

摘要

背景

中性粒细胞中的髓过氧化物酶可产生多种杀菌性氧化剂。本研究旨在阐明髓过氧化物酶基因多态性与胃癌发生之间的关系。

患者与方法

在一项对157例连续的胃癌患者和192例对照者的病例对照研究中,对髓过氧化物酶-463G→A基因多态性进行基因分型。此外,根据更新后的悉尼系统对胃黏膜变化进行检查。

结果

髓过氧化物酶A等位基因携带、男性、高龄、高盐饮食摄入及幽门螺杆菌感染独立增加胃癌风险[95%置信区间(CI):分别为1.5 - 5.0、1.7 - 6.5、2.6 - 8.6、1.1 - 2.6和1.2 - 3.8]。携带髓过氧化物酶A等位基因的幽门螺杆菌感染者发生肠型和弥漫型胃癌的风险均增加,比值比分别为7.9(95% CI 2.6 - 23.5)和8.6(95% CI 2.0 - 36.7)。在幽门螺杆菌感染个体中,A等位基因携带者胃窦部的细菌密度(p = 0.02)和中性粒细胞浸润评分(p = 0.05)高于非携带者,胃体部的中性粒细胞浸润评分(p = 0.02)和腺体萎缩评分(p = 0.03)也高于非携带者。

结论

本研究证实了髓过氧化物酶-463G→A基因多态性与胃癌的关联。这种基因多态性在胃癌发生中的潜在机制值得进一步研究。

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