ATDC在胃癌中的表达及其与幽门螺杆菌感染的关系

背景：ATDC又名TRIM29,属于TRIM蛋白家族,具有促进细胞增殖和抑制电离辐射敏感性的功能。研究显示其在某些恶性肿瘤中呈高表达,可作为胃癌淋巴结转移的标记,并参与了胰腺癌的生长和转移。目的：明确ATDC在胃癌中的作用,并初步探讨ATDC与幽门螺杆菌（H.pylori）相关胃癌的关系。方法：应用免疫组化方法检测72例胃癌患者癌组织和相应癌旁组织中的ATDC表达,分析其在胃癌组织中的表达与胃癌临床病理特征和患者H.pylori感染状态的关系。结果：胃癌组织ATDC阳性表达率显著高于相应癌旁组织（76.4%对2.8%,P〈0.05）。中低分化、伴淋巴结转移或远处转移、伴H.pylori感染的胃癌患者,胃癌组织ATDC阳性表达率和表达强度分别显著高于高分化、不伴转移、不伴H.pylori感染的胃癌患者（P〈0.05）,ATDC表达与胃癌患者的性别无关。结论：胃癌组织中的ATDC表达与胃癌组织学分级、转移和患者的H.pylori感染状态相关,提示其可能参与了胃癌的发生、发展,并可能与H.pylori相关胃癌有一定联系。     

胃癌中幽门螺杆菌感染与癌基因蛋白表达及凋亡

目的　研究幽门螺杆菌 (Hp)感染的胃癌 (GC)发展过程中c met蛋白表达与细胞凋亡的关系及对胃癌预后的意义。方法　对 14 5例经病理证实的不同胃粘膜病变采用免疫组化法检测c met基因表达及Warthin starry法检测Hp感染。采用原位末端标记法 (TUNEL)检测细胞凋亡。结果　在浅表性胃炎 (CSG)、萎缩肠化生胃炎 (CAG +IM )、异型增生 (DYS)、早期GC和进展期GC中 ,c met基因表达率分别为 2 5 .5 3 %、5 1.2 8%、6 1.5 4%、6 6 .6 7%和 6 8.42 % ,CAG +IM、DYS、GC的c met基因表达率均显著高于CSG (P <0 .0 5 )。凋亡指数 (AI)分别为( 4 .5 5± 2 .33) %、( 6 .43± 5 .6 0 ) %、( 6 .45± 5 .12 ) %、( 6 .5 5± 4.80 ) %和 ( 8.84± 5 .6 3) % ,进展期GC显著高于CSG(P <0 .0 5 )。胃粘膜凋亡指数与c met表达强度密切相关 (P <0 .0 5 )。c met阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关 ,而且BorrmannⅣ明显高于早期胃癌和BorrmannⅠ ,Ⅱ (P <0 .0 5 )。Hp阳性者 5年生存期显著短于Hp阴性者。 结论　Hp感染和c met表达与胃粘膜增殖和恶化有关 ,且与凋亡有相关性。Hp感染与胃癌预后有关。     

幽门螺杆菌与胃癌C-erb B-2表达的关系

目的探讨幽门螺杆菌(Hp)感染在胃癌中与C-erb B-2的关系.方法对27例胃癌、5例癌前病变和15例对照组应用Warthin-Starry染色法,免疫酶组化SP法检测C-erbB-2基因蛋白.结果 Hp感染率在胃癌和癌前病变组中均高于对照组,而前两组差异无显著性,Hp感染与C-erb B-2过度表达有关(P<0.05).结论 Hp感染可能作为促进剂使癌基因C-erb B-2激活,说明Hp感染在胃癌起一定作用.     

幽门螺杆菌感染宿主炎性因子基因多态性与胃癌的关系

幽门螺杆菌(Hp)感染被认为是胃癌发生发展的重要危险因素,而基因多态性可能是Hp感染导致不同结局的内在因素,此文综述了与Hp感染诱导的胃癌发病有关的宿主炎性因子的基因多态性。     

幽门螺杆菌感染对Fas/FasL表达的影响在胃癌发生中的作用

目的：观察幽门螺杆菌（Hp）及其不同毒力株（cagA阳性与cagA阴性株）感染对胃黏膜上皮细胞Fas/FasL表达的影响，进而探讨胃癌的发生机制。方法：胃镜下取胃窦黏膜标本，将研究对象按病理结果分为黏膜萎缩组，黏膜萎缩伴轻度不典型增生组，黏膜萎缩伴中度不典型增生组，胃腺癌组，黏膜大致正常组为对照组，再根据Hp感染情况为分Hp阳性组与阴性组，并将Hp阳性组进一步成cagA阳性组及阴性组，共9组80例。以快速尿素酶试验，PCR及组织学第三种方法检测Hp，用PCR方法对Hp进行分型。用免疫组化法检测Fas、FasL等表达情况。结果Hp感染率为60．0％，cagA阳性率为90．47％，非腺癌病人Hp阳性组Fas/FasL表达明显高于Hp阴性组（P＜0．05），腺癌组Fas/FasL表达明显高于大致正常组及黏膜萎缩，黏膜萎缩伴轻度不典型增生，黏萎缩伴中度不典型增生组（P＜0．01）。cagA阳性组Fas/FasL表达与cagA阴性组差异无显著性（P＞0．05）。结论：幽门螺杆菌感染后早期即黏 萎缩阶段已出现Fas、FasL等的表达增加，随细胞凋亡的增加，黏膜上皮细胞萎缩加重，细胞DNA不稳定性增加，并出现不典型增生加重， Fas、FasL的表达随之增强，一旦肿瘤细胞形成，Fas/FasL表达进一步增加，形成局部免疫豁免区，导致肿瘤的浸润生长。cagA阳性的菌株在促成肿瘤的发生过程中无明显作用。     

胃癌及癌前病变中幽门螺杆菌感染与Ezrin蛋白表达的关系

目的探讨细胞骨架蛋白Ezrin在胃癌、癌前病变中的表达与Hp感染关系,及其在胃癌发生发展中可能的机制。方法采用免疫组化方法检测49例胃癌及癌前病变组织及16例正常胃黏膜标本中Ezrin蛋白的表达情况,并用快速尿素酶试验或Warthin．Starry胃螺旋染色法检测幽门螺杆菌（Hp）感染。结果胃癌及癌前病变组织Hp感染率显著高于正常组织（P〈0．01）;Ezrin蛋白表达在正常胃组织、癌前病变组织和胃癌组织中呈递减趋势,三者比较差异有统计学意义（P均〈0．05）;胃癌组织及癌前病变组织中Hp感染阳性组Ezrin蛋白的表达显著低于阴性组（P〈0．05）。结论在胃黏膜癌变过程中,Ezrin蛋白表达逐渐下调,Ezrin蛋白表达与Hp感染相关,提示Hp感染可通过影响Ezrin蛋白表达,在胃癌的发生发展过程中发挥一定作用。     

环氧化酶-2在胃癌和胃炎中的表达及其与幽门螺杆菌感染的关系

目的探讨环氧化酶-2（Cyclooxygense-2，COX-2）在胃癌和胃炎中的表达及其与幽门螺杆菌（Helicobacter pylori，Hp）感染的关系，为胃癌的预防和治疗提供有价值的实验和理论依据。方法采用免疫组化技术检测COX-2、Hp在胃癌以及各型胃炎中的表达。结果胃癌和萎缩性胃炎伴不典型增生组织中COX-2的表达率明显高于浅表性胃炎（P〈0.05），COX-2在Hp感染阳性萎缩性胃炎伴不典型增生病人中的表达率明显高于Hp感染阴性组（P〈0．05），高、中分化胃癌COX-2表达率高于低分化胃癌（P〈0．05）。结论COX-2在胃癌组织中存在过表达，Hp感染可使萎缩性胃炎伴不典型增生组织中COX-2表达增强，COX-2表达与胃癌分化程度有关。     

幽门螺杆菌感染与心脑血管病的关系研究进展

近年来幽门螺杆菌(helicobacter pylori,HP)感染与其消化道疾病胃炎、消化性溃疡、胃黏膜相关淋巴组织淋巴瘤、胃癌等关系的研究,已取得了长足的进展,与胃肠外疾病探讨也处于热点之中。随着研究的深入,发现心脑血管病等与HP感染也存在着密切的联系,现将其作一综述。1冠心病1.1H     

cag Ⅱ在慢性胃病患者感染幽门螺杆菌中的检出及其与疾病的关系

目的:探讨新近发现的毒力相关因子基因群集的左半部分——cag Ⅱ在慢性胃病患者感染幽门螺杆菌(H·pylori)中的检出率及其与H·pylori致病的相关性。方法:采用PCR方法,在107例慢性胃病患者中分离的H·pylori菌株,分别扩增cag Ⅱ中的597pb片段。结果:cag Ⅱ的阳性检出率为69.2 ％,在慢性胃炎、消化性溃疡、胃癌等疾病间的检出无显著差异(P>0.05)。结论:cag Ⅱ在慢性胃病患者不同疾病感染的H·pylori中均有检出。在慢性胃炎、消化性溃疡、胃癌等疾病间的检出率无明显差异,表明cag Ⅱ基因在慢性胃病患者感染H·pylori中的分布与H·pylori毒力的关系并不十分密切,cag Ⅱ的存在意义还有待于进一步研究。     

幽门螺杆菌感染与C-myc基因和P53基因表达与胃癌的相关性研究

目的探讨幽门螺杆菌（Hp）感染情况与C-myc基因及P53基因的表达与胃癌的相关性。方法用w—s染色法观察不同胃病黏膜组织中Hp感染情况，采用免疫组化检测技术检测不同胃病组织的C-myc基因和P53基因表达产物。结果胃癌及癌前病变组Hp感染率明显高于慢性浅表性胃炎组（P〈0．01），C-myc基因和P53基因的表达也显著高于慢性浅表性胃炎组（P〈0．01）。Hp感染阳性组的C-myc基因和P53基因表达明显高于Hp感染阴性组（P〈0．01）。结论Hp感染可能通过激活C-myc基因，同时使P53基因失活从而诱发胃黏膜的癌变。     

胃癌及癌前病变组织中幽门螺杆菌感染与视网膜母细胞瘤基因表达的相关性研究

目的 探讨胃癌和胃黏膜癌前病变组织中幽门螺杆菌(Hp)感染和视网膜母细胞瘤基因(Rb基因)的表达及两者的相关性.方法 采用免疫组化S-P法检测19例慢性浅表性胃炎(CG)、20例胃黏膜不典型增生(Dys)和41例胃癌组织标本(Gc)中Rb蛋白的表达,并采用War-thin-Starry细菌染色及免疫组化S-P法检测Hp感染率.结果 慢性浅表性胃炎Hp感染率(36.8%)明显低于不典型增生组(70.0%)和胃癌组(65.9%),P<0.05.胃癌中Rb阳性表达率(48.8%)明显低于胃炎组(94.7%)及不典型增生组(80.0%),P<0.05.胃癌中Hp感染与Rb阳性表达呈明显负相关(P<0.01).结论 Hp感染可能在胃癌发生中起重要作用,Hp感染可能通过诱导Rb基因突变从而导致胃癌的发生.     

幽门螺杆菌感染与胃癌的相关性研究

目的：为了研究幽门螺杆菌（Hp）感染与胃癌及肠化类型的关系。方法：对胃癌高发区1333例普查人群的胃活检组织和30例胃癌手术标本病理切片做Warthin－starry染色，对慢性萎缩胃炎伴肠化生、慢性浅表胃炎伴肠化生、癌旁肠化生用粘液组化方法染色分型。结果：Hp感染与十二指肠球部溃疡高度相关，与胃溃疡、慢性浅表活动性胃炎、早期胃癌显著相关，与单纯萎缩性胃炎、萎缩胃炎伴肠化生、胃增生性息肉亦相关（P均＜0．05）；进展期胃癌的Hp感染率与慢性非活动性胃炎相比较，差异无显著性（P＞0．05）；各型胃癌中以腺癌Hp检出率高（75．4％），与粘液细胞癌Hp检出率（30％）相比较，差异有非常显著性（P＜0．01）。各型肠化生之间的Hp检出率比较，差异无显著性（P均＞0．05）。结论：Hp感染与胃癌有相关性。     

胃癌变过程中Hp感染与凋亡基因Survivin表达的关系

目的 研究胃癌变过程中幽门螺杆菌（Hp）感染与凋亡基因Survivin表达、细胞凋亡的关系。方法用快速尿素酶法、W—S银染法和美蓝法联合检测62例慢性浅表性胃炎（CSG）、55例慢性萎缩性胃炎（CAG）、52例肠化生（IM）、46例不典型增生（AH）、65例胃癌（Gc）组织中Hp的感染情况,采用免疫组化及TUNEL法分别检测Survivin蛋白的表达及细胞凋亡情况。结果Hp感染率、Survivin蛋白阳性表达率均随着GC形成中病变恶性程度的加重而明显上升（P〈0．05）。CAG、IM、AH和GC组Hp感染率较CSG组,Gc组较CAG组均明显升高（P均〈0．05）;AH、GC组Survivin蛋白阳性表达率明显高于IM和CAG组（P均〈0．01）;AH、GC组Hp阳性患者Survivin蛋白表达率均高于Hp阴性者（P均〈0．05）;CAG、IM、AH、GC组中Survivin阳性者凋亡指数均低于Survivin阴性者（P〈0．05）;低未分化GC患者Survivin蛋白表达明显高于高中分化者（P均〈0．05）。结论在胃黏膜癌变过程中,Hp感染可能通过逐渐上调Survivin基因的表达、抑制细胞凋亡和分化而发挥致癌作用。     

Preferential expression of cyclooxygenase-2 in colonic-phenotype of gastric intestinal metaplasia: association with helicobacter pylori and gastric carcinoma

OBJECTIVES: Gastric intestinal metaplasia (GIM) associated with H. pylori (HP) has been considered a premalignant lesion. However, GIM phenotype associated with HP infection and gastric cancer is unclear. The expression of COX-2 in relation to GIM phenotype is also unknown. METHODS: We evaluated cellular phenotype and COX-2 expression in the GIM from HP-positive and -negative patients from Japan in the absence of gastric cancer (n = 31) by using a colon epithelium specific monoclonal antibody (mAb Das-1) and anti-COX-2 antibody. COX-2 expression was also examined in patients with gastric cancer (n = 34), both in the cancer and in the GIM areas away from the cancer field. RESULTS: Sixty-eight percent of HP-positive GIM reacted with mAb Das-1, whereas the reactivity in the HP-negative GIM was only 25% (P < 0.001). The COX-2 expression was present in 32% of HP-positive GIM and in only 9% of HP-negative GIM (P < 0.001). In the cancer group, COX-2 expression was localized both in the cancer area (94%) and in the GIM (82%) away from the cancer. Each of the COX-2-positive tissue was also positive to mAb Das-1. CONCLUSION: HP infection is highly associated with the development of colonic-phenotype of GIM, and about half of them expressed COX-2. COX-2 expression was frequent in both gastric cancer and the GIM adjacent to the cancer. The results suggest that the presence of mAb Das-1 and COX-2 reactivity in the GIM identify the subgroup of patients who may be at risk for gastric cancer and may need close surveillance.     

地区差异与老年人幽门螺杆菌感染的相关性

目的了解北京地区老年人群中幽门螺杆菌（Hp）的感染状况和地区差异。方法采用随机抽样人户问卷调查的方法，调查北京不同地区（城区、郊区、山区）60岁及以上的老人2006例，应用免疫印迹法检测血清Hp-IgG抗体。结果山区老人Hp的感染率为91．1％。城区为82．6％，郊区为77．2％，山区明显高于城区和郊区（P〈0．001）。结论北京城区、郊区和山区老年人群中的Hp感染率存在着显著差异，但地理因素不是决定性因素。     

New approaches to helicobacter pylori infection in children

Helicobacter pylori infection is usually acquired during childhood, and evidence-based guidelines regarding diagnosis and treatment of infected children have been recently published. Diseases associated with H. pylori infection are gastritis, duodenal ulcers, mucosal-associated lymphoid-type (MALT) lymphoma, and gastric adenocarcinoma. The association of specific symptoms with H. pylori infection in children and adults (ie, recurrent abdominal pain and nonulcer dyspepsia) remains controversial. Additionally, the role of H. pylor in gastroesophageal reflux disease or in extra-gastrointestinal diseases (ie, coronary artery disease) lacks sufficient evidence to demonstrate causality. The diagnosis of H. pylori-associated diseases in children can reliably be made through gastroduodenal endoscopy with biopsies. Clinical trials are underway for the validation of noninvasive diagnostic tests for the H. pylori-infected child, and current guidelines recommend eradication therapy for infected children with duodenal and gastric ulcer, gastric lymphoma, and atrophic gastritis with intestinal metaplasia. The natural history of childhood H. pylori infection is poorly described. Moreover, rational approaches to the prevention and control of childhood H. pylori infection are critically needed, requiring characterization of the determinants for acquisition and persistence and the disease outcomes following eradication.     

Epidemiology of gastric cancer in relation to diet and Helicobacter pylori infection

Abstract Gastric cancer is the second most common fatal malignancy in the world. In China, gastric cancer is now the second most common malignancy, while in Hong Kong, the mortality rate ranked fourth among all cancers in 1995. Dietary factors in gastric carcinogenesis came mostly from case-control studies. N-Nitroso compounds from dietary sources such as preserved, smoked and salted foods were found to be associated with gastric cancer. ß-Carotene, selenium and α-tocopherol have been shown in an intervention study to be favourable in the reduction of stomach cancer mortality. Fruits and vegetables showed the most consistent results of inverse association with gastric cancer. Dietary salt intake in preserved or salted foods is also shown to be associated with gastric cancer. Tea drinking, especially green tea, has a protective effect against gastric cancer as shown in some studies. Prospective case-control studies of the association between Helicobacter pylori infection and the subsequent development of gastric cancer showed that the odds ratio ranged from 2.8 to 6.0. However, results of similar case-control studies in countries with a high frequency of gastric cancer are controversial. Infection with H. pylori leads to changes in the vitamin C content of gastric juice, reactive oxygen metabolites, epithelial cell proliferation and apoptosis. Recently, CagA-positive strains were found to be associated with gastric cancer and also duodenal ulcers. The exact role of H. pylori in gastric carcinogenesis is still under investigation. Large-scale intervention studies are underway to examine dietary supplementation, H. pylori infection and gastric cancer. Helicobacter pylori eradication for gastric cancer prevention is being conducted in China and other parts of the world. In high-risk areas, for example in China, a combination approach including H. pylori eradication and dietary supplementation may be necessary.