Inducible nitric oxide synthetase genotype and Helicobacter pylori infection affect gastric cancer risk

作     者：Alireza Rafiei Vahid Hosseini Ghasem Janbabai Bahman Fazli Abulghasem Ajami Zahra Hosseini-khah Jeremy J Gilbreath D Scott Merrell 

作者机构：Faculty of MedicineMolecular and Cell Biology Research CenterMazandaran University of Medical Sciences Department of Internal MedicineMazandaran University of Medical Sciences Department of Internal MedicineImam HospitalMazandaran University of Medical Sciences Department of Microbiology and ImmunologyUniformed Services University of the Health Sciences 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2012年第18卷第35期

页      面：4917-4924页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Supported by The Mazandaran University of Medical Sciences No. 88-512 

主　　题：Inducible nitric oxide synthetase Gastriccancer Helicobacter pylori Heterozygous CT geno-type Homozygous -IF genotype 

摘      要：AIM： To investigate the association of the inducible ni- tric oxide synthetase （iNOS） C150T polymorphism with Helicobacter pylori （H. pylor/） infection and gastric can- cer （GC） risk in Iran. METHODS： In order to determine whether there was a correlation between iNOS genotype and GC in Iran, we conducted a case-control study using samples from 329 individuals. For each sample, the C150T ilVOS poly- morphism was genotyped by polymerase chain reaction （PCR） and restriction digestion. Patients were grouped by cancer presence, demographic and behavior charac- teristics, and/-/, pylori infection status. Statistical tests were conducted to determine whether any behavioral factors or a particular iNOS genotype was associated with GC in the study population. RESULTS： In this population, we found that smok- ing, hot beverage consumption, a familial history of GC and H. pylori infection status were significantly associated with GC development （P = 0.015, P 〈 0.001, P = 0.0034, and P 〈 0.015, respectively）. The distribution of the C150T ilVOS genotypes among the two study groups was not statistically significant alone, but was impacted by H. pylori infection status. When compared to the non-/-/, pylori infected group, cancer patients who had a heterozygous CT genotype and were also infected with H. pylori were 2.1 times more at risk of developing GC [odds ratio （OR） = 2.1, P = 0.03] while those with a homozygous TT genotype and infected with H. pylori were 5.0 times more at risk of developing GC （OR = 5.0, P = 0.029）. In contrast, this association was not seen in patients in the control ***： ACT or TT polymorphism at position 150 in the iNO$ gene significantly increases the risk of GC and may be a marker for GC susceptibility.