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| 1 | Host pathogen interactions in Helicobacter pylori related gastric cancer显示文摘Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group?Ⅰ?carcinogen since this bacterium is responsible for the highest rate of cancerrelated deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinaltype gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor. | Magdalena Chmiela Zuzanna Karwowska Weronika Gonciarz Bujana Allushi Pawel Staczek | 2017 | World Journal of Gastroenterology2017，23，9： | 37 |
| 2 | 化浊解毒方治疗慢性萎缩性胃炎伴幽门螺杆菌感染患者的临床研究显示文摘目的观察化浊解毒方治疗浊毒内蕴证慢性萎缩性胃炎(CAG)伴幽门螺杆菌感染(Hp)患者的Hp根除率及临床疗效,探讨其可能的作用机制。方法将120例CAG伴Hp感染患者随机分为治疗组和对照组各60例。治疗组予化浊解毒方口服,每日1剂;对照组先予标准四联杀菌疗法服用2周,继予安慰剂口服,每日1剂。治疗3个月后比较2组治疗前后的中医证候积分、胃镜黏膜征象积分、病理学组织改变积分、胃泌素-17(G-17)、血清胃蛋白酶原Ⅰ、Ⅱ(PGⅠ、PGⅡ)、PGⅠ/PGⅡ比值(PGR)、细胞毒素相关蛋白(CagA)、空泡细胞毒素(VacA)及尿素酶B(UreB)水平变化;治疗前、治疗6周、治疗3个月记录Hp根除率,并随访6个月,观察Hp的复发情况。结果治疗后,2组中医证候积分均较治疗前降低(P<0.05~0.01),优于对照组(P<0.05~0.01)。治疗组的胃镜黏膜征象积分、病理学组织改变积分均较治疗前降低(P<0.05~0.01),优于对照组(P<0.01)。治疗组PGⅠ、PGR水平较治疗前升高,PGⅡ、G-17水平较治疗前降低(P<0.05~0.01),优于对照组(P<0.05~0.01)。2组CagA、VacA及UreB的阳性率均较治疗前明显降低(P<0.01),优于对照组(P<0.05~0.01)。治疗组Hp根除率优于对照组(P<0.05~0.01)。随访6个月,治疗组复发率低于对照组(P<0.01)。结论化浊解毒方治疗浊毒内蕴证CAG伴Hp感染,抑杀Hp效果好,复发率低,且可有效缓解临床症状、改善病理组织学病变、促进黏膜修复,其治疗CAG的作用机制可能与影响CagA、VacA、UreB、PGⅠ、PGⅡ、PGR及G-17的水平相关。 | 白海燕 郝旭蕊 李娜 刘凯娟 李维康 杨倩 | 2020 | 南京中医药大学学报2020，36，3： | 31 |
| 3 | Cytokines,cytokine gene polymorphisms and Helicobacter pylori infection:Friend or foe?显示文摘Helicobacter pylori(H.pylori)is a flagellated,spiralshaped,microaerophilic Gram-negative bacillus that colonises the gastric mucosa of more than 50%of the human population.Infection is a risk factor for gastritis,ulcer disease and stomach cancer.Immunity against H.pylori is mainly related to Th1/Th17 skewing,and the activation of regulatory T cells is the main strategy used to limit inflammatory responses,which can result in the pathogen persistence and can lead to chronic gastrointestinal diseases,including cancer.Furthermore,host genetic factors that affect cytokines may determine differences in the susceptibility to many diseases.In this review,we present the cytokine profiles and the main cytokine gene polymorphisms associated with resistance/susceptibility to H.pylori and discuss how such polymorphisms may influence infection/disease outcomes. | Camila A Figueiredo Cintia Rodrigues Marques Ryan dos Santos Costa Hugo Bernardino F da Silva Neuza M Alcantara-Neves | 2014 | World Journal of Gastroenterology2014，20，18： | 11 |
| 4 | Role of gene polymorphisms in gastric cancer and its precursor lesions:Current knowledge and perspectives in Latin American countries显示文摘Latin America shows one of the highest incidence rates of gastric cancer in the world,with variations in mortality rates among nations or even within countries belonging to this region.Gastric cancer is the result of a multifactorial complex process,for which a multistep model of carcinogenesis is currently accepted.Additionally to the infection with Helicobacter pylori,that plays a major role,environmental factors as well as genetic susceptibility factors are significant players at different stages in the gastric cancer process.The differences in population origin,demographic structure,socio-economic development,and the impact of globalization lifestyles experienced in Latin America in the last decades,all together offer opportunities for studying in this context the influence of genetic polymorphisms in the susceptibility to gastric cancer.The aim of this article is to discuss current trends on gastric cancer in Latin American countries and to review the available published information about studies of association of gene polymorphisms involved in gastric cancer susceptibility from this region of the world.A total of 40 genes or genomic regions and69 genetic variants,58%representing markers involved in inflammatory response,have been used in a number of studies in which predominates a low number of individuals(cases and controls)included.Polymorphisms of IL-1B(-511 C/T,14 studies;-31 T/C,10 studies)and IL-1RN(variable number of tandem repeats,17 studies)are the most represented ones in the reviewed studies.Other genetic variants recently evaluated in large metaanalyses and associated with gastric cancer risk were also analyzed in a few studies[e.g.,prostate stem cell antigen(PSCA),CDH1,Survivin].Further and better analysis centered in gene polymorphisms linked to other covariates,epidemiological studies and the information provided by meta-analyses and genome-wide association studies should help to improve our understanding of gastric cancer etiology in order to develop appropriate health programs in Latin America. | Miguel Angel Chiurillo | 2014 | World Journal of Gastroenterology2014，20，16： | 6 |
| 5 | 幽门螺杆菌在胃癌发病机制中的作用研究显示文摘幽门螺杆菌(Hp)是人类医学上感染率最高的细菌之一,是导致慢性胃炎的直接病因,临床上证实其与胃、十二指肠溃疡和胃癌发病机制密切相关。目前国内外对Hp感染的危险因素进行了大量的临床研究。1994年世界卫生组织(WHO)/国际癌症研究机构(LARC)确定Hp为I类致癌因子。Hp之所以对人体消化道造成重大危害,是因为它可以产生很多附带的毒性因子。 | 杨宗澄 李思捷 | 2014 | 安徽医药2014，18，8： | 6 |
| 6 | 幽门螺杆菌主要毒力因子及其与胃癌关系的研究进展显示文摘幽门螺杆菌(Hp)感染被定义为感染性疾病已在全球达成共识,其与胃癌的发生、发展密切相关,本文将从Hp主要毒力因子VacA、CagA与胃癌的关系,根除Hp感染对预防胃癌及其机制的研究进展作一综述。 | 刘榕 高孝忠 | 2019 | 中华胃肠内镜电子杂志2019，6，3： | 6 |
| 7 | 幽门螺杆菌毒力基因与胃癌的研究进展显示文摘 | 林妙端 佘菲菲 | 2009 | 福建医科大学学报2009，43，3： | 4 |
| 8 | 幽门螺杆菌的毒力因子分型及与胃肿瘤的相关性分析显示文摘目的探讨幽门螺杆菌(Hp)的各型毒力因子与胃肿瘤发生发展的相关性。方法以生物芯片技术,PCR技术及Southern杂交和Western免疫印迹法等对Hp的各型毒力因子的基因进行分型,根据不同基因型毒力因子在胃肿瘤中的生物学作用,分析它们与肿瘤的发展可能的相关性。结果世界各地开展了大量关于Hp基因多态性与胃癌发生的研究,然而尚未有哪个毒力基因或其亚型作为明确的胃癌危险因素被证实,且不同的研究报道的结果并不完全一致,许多问题仍存在争议,对这些致癌基因的作用机制及其与胃癌的关系有待进一步研究。胃癌的发生是一个多病因多阶段的过程,Hp作为胃癌的I类致癌因子,其致癌机理是一个多因素、多阶段、多基因变异参与的过程,除了考虑为地区人种遗传基因的变异及环境因素的不同外,还应考虑不同地区幽门螺杆菌的感染率及基因亚型分布的差异为可能因素。结论有关Hp毒力基因及其致恶变方面研究进展很快,基础研究方面的突破,特别是对可塑区的研究技术上的突破,将大大推动临床根除Hp及Hp相关性胃腺癌和胃MALT淋巴瘤的预防及治疗。 | 张亚琼 章月桃 | 2013 | 黑龙江医学2013，37，6： | 3 |
| 9 | 新疆乌鲁木齐幽门螺杆菌基因分型与萎缩性胃炎的相关性分析显示文摘目的探讨新疆乌鲁木齐幽门螺杆菌(Helicobacter pylori,Hp)基因分型与萎缩性胃炎的相关性。方法选取2016年6月至2017年6月在我院消化科诊断为慢性胃炎且C14阳性的310例患者,萎缩性胃炎患者150例,非萎缩性胃炎患者160例。记录2组一般资料,胃镜及病理、C14、分型检测结果。结果两组一般资料差异无统计学意义(P>0.05)。HP不同抗体阳性率相比较,萎缩性胃炎组较高。两组Cag A-128、VacA-110、VacA-90的阳性率统计学有差异(P<0.05)。HP的CagA-128、VacA-110、VacA-90与萎缩性胃炎患者相关,与CagA-128相关密切;CagA-128、VacA-110是慢性萎缩性胃炎发生的相关危险因素。结论新疆乌鲁木齐HP基因分型CagA基因、VacA基因与萎缩性胃炎发生密切相关,检测HP基因表达抗体对鉴别诊断有一定指导意义,为'因型治病'提供依据。 | 杨丽君 柯月 孟清 丁永年 | 2018 | 世界最新医学信息文摘2018，18，34： | 1 |
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