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。     

幽门螺杆菌与胃癌

胃癌是严重危害人类健康的最常见的恶性肿瘤之一,在世界上的恶性肿瘤中估计占第二位。我国胃癌年死亡率为16/10万,居各类恶性肿瘤之首。近20年来,不少学者致力于胃癌流行病学研究,发现胃癌的发生与环境因素有关。自1983年从人胃粘膜中分离出幽门螺杆菌(Helicobacter Pylori,HP)以来,许多研究认为该菌感染作为环境因素之一,与胃癌的发生有关。虽然尚不能肯定两者有因果关系,但越来越多的资料支持HP在胃癌的发生中起一定的作用。本文就近年来流行病学资料,从病因学研究的原则角度,对HP与胃癌的病因学关系作一综述。     

在唾液中检测幽门螺杆菌的意义

探讨一种有效的非侵入性幽门螺杆菌诊断方法。方法１３８／１５９例各类型胃、十二指肠疾病患者的唾液和胃黏膜,用空泡毒素基因为模板设计的引物行聚合酶链反应,其产物行单链构象多态性分析和Ｓｏｕｔｈｅｒｎ杂交。     

免疫组织化学技术在幽门螺杆菌研究中的应用

自从 1983年Ｍａｒｓｈａｌｌ分离培养出幽门螺杆菌(Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ,简称Ｈｐ)以来 ,大量研究表明 ,Ｈｐ与慢性胃炎、消化性溃疡、胃癌的发生有密切关系。目前Ｈｐ的研究 ,已经从传统的形态学发展到分子生物学水平 ,也发展了一系列技术方法 ,如形态学观察、组织染色、免疫组织化学染色、ＰＣＲ等。由于免疫组织化学技术具有特异性强、定位准确、形态与功能相结合等特点 ,在Ｈｐ的研究中占有重要地位。现将免疫组织化学技术在Ｈｐ检测、流行病学调查和致病机理三个方面的探讨作一综述。1　免疫组织化学用于Ｈｐ的检测1…     

幽门螺杆菌和胃癌

胃癌是常见的恶性肿瘤之一,近些年由于人们对胃癌的预防、早期诊断及治疗越来越重视,其发病率和病死率呈下降趋势,近10年间下降约10%[1]。但胃癌仍为世界上第四大肿瘤,病死率位居恶性肿瘤的第二位[1]。流行病学和动物实验等均证实幽门螺杆菌(helicobacter pylori,Hp)感染可增加胃癌发病的危险性。1994年WHO国际癌症研究中心将     

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。     

幽门螺杆菌感染与胃癌

幽门螺杆菌感染与胃癌梁后杰，刘为纹临床和实验研究表明幽门螺杆菌（ＨＰ）是慢性胃炎的病原菌，在消化性溃疡的复发中也起着重要作用，但与胃癌的关系尚不完全清楚，本文仅就ＨＰ感染与胃癌关系的研究现状作一综述。一、流行病学调查１．年龄分布一致性胃癌的发病享随年...     

幽门螺杆菌相关microRNA在胃癌中的作用

已有研究提示微小RNA(miRNA)参与了多种肿瘤包括胃癌的发生、发展,幽门螺杆菌(Hp)与胃癌发生、发展关系密切。近期研究表明Hp可能通过miRNA途径促进胃癌的发生、发展。本文就胃癌相关miRNA,尤其是Hp感染相关miRNA分子及其作用机制作一综述。     

幽门螺杆菌粪便抗原检测在幽门螺杆菌感染诊断及随访中的价值

目的 对幽门螺杆菌粪便抗原（HpSA）检测诊断hp感染、hp根除治疗后的随访及在儿童中的应用价值,进行临床评价。方法 以快速尿素酶试验=、组织学和细菌培养中的二项阳性或细菌培养一项阳性作为诊断HP的金标准,采用ELISA法检测128例因上消化道症状接受胃镜检查患者HPSA,评价HPSA诊断HP感染的敏感性、特异性;其中79例同时进行^13C-UBT作为对照,评价HPSA诊断HP感染的准确性。结果 在128例中,HPSA检测的敏感性、特异性和准确性分别为95.16%,98.41%和96.80%。根除治疗前HPSA检测和^13C-UBT诊断HP的敏感性为97.96%和95.92%,特异性为96.67%和100.00%,准确性均为97.46%;根除治疗后4周随访HPSA检测和^13C-UBT的敏感性均为100.00%,特异性为91.43%和94.29%,准确性 93.18%和95.45%。以^13C-UBT作标准,HPSA检测29例患儿HP感染敏感性、特异性和准确性分别为91.67%,88.23%和89.66%。结论 HPSA检测是一种简便、准确、非侵入性的诊断HP感染的方法,适用于HP感染的诊断、根除治疗后随访及儿童患者。     

Dynamic expression of pepsinogen C in gastric cancer, precancerous lesions and Helicobacter pylori associated gastric diseases

AIM: To investigate the relationship between the expression of pepsinogen C (PGC) and gastric cancer, precancerous diseases, and Helicobacter pylori (H pylori) infection. METHODS: The expression of PGC was determined by immunohistochemistry method in 430 cases of gastric mucosa. H3 Pylori infection was determined by HE staining, PCR and ELISA in 318 specimens. RESULTS: The positive rate of PGC expression in 54 cases of normal gastric mucosa was 100%. The positive rates of PGC expression in superficial gastritis or gastric ulcer or erosion, atrophic gastritis or gastric dysplasia and gastric cancer decreased significantly in sequence (P<0.05; 100%/89.2% vs 14.3%/15.2% vs 2.4%). The over-expression rate of PGC in group of superficial gastritis with H pyloriinfection was higher than that in group without H pylori infection (P<0.05; x2= 0.032 28/33 vs 15/25). The positive rate of PGC expression in group of atrophic gastritis with H pylori infection was lower than that in group without H pylori infection (P<0.01; x2 = 0.003 4/61 vs9/30), and in dysplasia and gastric cancer. CONCLUSION: The level of PGC expression has a close relationship with the degree of malignancy of gastric mucosa and development of gastric lesions. There is a relationship between H pylori infection and expression of antigen PGC in gastric mucosa, the positive rate of PGC expression increases in early stage of gastric lesions with H pylori infection such as gastric inflammation and decreases during the late stage such as precancerous diseases and gastric cancer. PGC-negative cases with H py/ori-positive gastric lesions should be given special attention.     

Helicobacter pylori and gastric cancer

Infection with Helicobacter pylori is now recognized as the primary cause of peptic ulcers and their recurrence. Compelling evidence has also been found linking H. pylori infection to gastric cancer, the second most common cancer in the world. Given the high rate of patient morbidity and mortality associated with gastric cancer, any method by which one can reduce the occurrence of the disease or increase its early detection is desirable. The strong correlation with H. pylori infection and the current availability of easily administered tests for the detection of the pathogen argue for screening at least those individuals with a family history of gastric cancer or other risk factors. This article reviews the association between H. pylori and gastric cancer and the pathologic changes that the infection produces in the gastric mucosa, as well as the cost-effectiveness of universal testing and eradication of the infection in H. pylori-positive individuals to reduce gastric cancer.     

Helicobacter pylori and gastric cancer

Gastric cancer despite a declining incidence remains a significant cause of morbidity and mortality world wide. There is strong epidemiological and histological evidence to associate Helicobacter pylori infection with the subsequent development of gastric cancer. The exact pathophysiological mechanisms involved remain to be elucidated. There is evidence to relate Helicobacter pylori infection and subsequent inflammation with an increase in gastric epithelial cell proliferation and with the induction of apoptosis. Such alterations in cellular dynamics may promote the development of mitogenic cell lines by inducing DNA damage. Studies have shown that following successful treatment, proliferation rates return to normal. At what histological stage, eradication is of benefit is less clear. It is likely that following the development of atrophy or intestinal metaplasia eradication will only slow progression. It would, therefore, seem logical, that to establish any benefit for a population, treatment should be employed at an earlier stage. As yet, an at risk group has not been identified, and as such population screening cannot be advised, mainly as a result of financial implications and the risk of promoting the development of resistant strains. Recent studies have explored the rules of bacterial factors, CagA and VacA status, host factors, HLA type, and environmental factors as determinants of outcome. Results have been variable. The establishment of an at risk group would enable selective screening and treatment, and thus prevent the development of gastric carcinoma as a result of Helicobacter pylori infection in the long-term.     

Helicobacter pylori and gastric cancer

Abstract This review focuses on the similarities between the epidemiology of gastric cancer and the epidemiology of Helicobacter pylori. Their demographic patterns and the results of studies regarding familial and environmental risk factors are described. The association of gastric cancer and H. pylori infection with both gastric ulcer and chronic atrophic gastritis is also characterized and the possibility that a H. pylori infection could lead to gastric cancer is discussed.     

幽门螺杆菌感染在胃癌及癌前病变中的研究

目的　研究胃癌及癌前病变与Hp感染的关系 ,以探讨Hp可能的致癌机制。 方法　经内镜和病理明确诊断的胃癌及癌前病变者共 5 48例 ,包括慢性浅表性胃炎 (CSG) 16 3例、慢性萎缩性胃炎 (CAG) 2 0 7例、肠上皮化生 (IM) 71例 ,异型增生(DYS) 4 5例及胃癌 (GC) 6 2例。每例均活检胃窦大小弯、胃角及胃体大小弯共 5块 ,以WS法检测Hp。结果　癌前病变及胃癌Hp感染均较高 ,CAG(4 2 .5 % ) ,IM(76 .1% ) ,DYS(88.9% )和GC(72 .5 % ) ,与CSG(2 3.9% )有显著性差异 (P <0 .0 5或P <0 .0 1)。随着年龄增大 ,CAG、IM、DYS和GC逐步增多 ,而且≥ 5 6岁年龄组IM、DYS和GC显著多于≤ 40岁组 (P <0 .0 5 ) ,但CSG则相反。肠型胃癌和Hp感染密切相关 (P <0 .0 5 ) ,从胃窦小弯和大弯、胃角及胃体小弯和大弯顺序 ,Hp感染随着CSG、CAG、IM、DYS和GC病变而增高 ,Hp感染部位也在上移 ,尤其在胃体小弯及大弯 ,IM、DYS和GC的Hp感染显著高于CSC部位 (P <0 0 5 )。结论　Hp感染是导致从胃炎→胃萎缩→肠化→异型增生→癌变序列发展的危险因子 ,肠型胃癌和Hp感染密切相关 ,胃镜检查应该多部位取活检作病理及Hp检测 ,尤其是高位