幽门螺杆菌与大肠癌的关系

1982年4月,澳大利亚学者Marshall和Warren成功地从人胃粘膜组织中培养出幽门螺杆菌(Helicobacter Pylori,Hp)[1].1994年,世界卫生组织国际癌症研究机构(IARC)将Hp定为一级致癌物,并且认为Hp感染与胃癌有关[2].随着人们对Hp研究的进一步加深,许多学者发现Hp除了与胃溃疡和胃癌有关外,也与其他疾病有一定关系,例如:胃粘膜相关性淋巴细胞组织(MALT)淋巴瘤[3]、大肠癌[4]、缺血性心脏病[5]等.     

幽门螺杆菌感染与血液系统疾病的相关性研究进展

摘 要：世界人口幽门螺杆菌（Helicobacter pylori,Hp）感染超过50%,是人类最常见的细菌感染。幽门螺杆菌最常感染的部位是消化系统。随着研究的不断深入,除消化系统疾病外,多种血液系统疾病也被证实与Hp感染有关,其中包括缺铁性贫血（iron-deficiency anemia,IDA）、巨幼细胞性贫血（megaloblastic anemia,MA）、特发性血小板减少性紫癜（idiopathic thrombocytopenic purpura,ITP）、过敏性紫癜（allergic purpura,AP）、胃黏膜相关性淋巴组织（mucosa-associated lymphoid tissue,MALT）淋巴瘤等。以上血液系统疾病患者Hp感染率普遍高于正常人,并且在根除Hp后,上述血液系统疾病的临床症状分别得到不同程度的缓解甚至痊愈,提示Hp通过不同机制影响上述血液系统疾病的发生、发展。     

幽门螺杆菌致胃癌相关因素研究进展

幽门螺杆菌已被世界卫生组织国际癌症研究机构列为胃癌的第一类致癌物.虽然全世界超过半数人口感染幽门螺杆菌,但最终发展为胃腺癌者仅占感染人群的1％～3％.近年来的观点认为,胃癌是一种感染性疾病,毒力因子、宿主遗传因素和环境因素共同影响着幽门螺杆菌的致胃癌作用.其中,毒力因子在致胃癌初始发生的相关免疫反应中起重要作用,宿主遗传因素可影响炎性反应的严重度并可能加重胃黏膜损伤,而环境因素则可能改变幽门螺杆菌感染的临床结局.本文就幽门螺杆菌致胃癌相关因素的最新研究进展进行综述.     

幽门螺杆菌感染和maspin基因表达与胃癌相关性的研究

目的:探讨幽门螺杆菌(Hp)感染和maspin基因表达与胃癌发生发展的关系。方法:Grams染色和改良W-S银染法观察65例浅表性胃炎、58例癌前病变和79例胃癌黏膜组织中Hp感染情况,免疫组化技术检测不同胃黏膜组织maspin基因表达产物。结果:胃癌组、癌前病变组Hp感染率分别是79.7%(63/79)、58.6%(34/58),均明显高于慢性浅表性胃炎组的30.8%(20/65),χ2值分别为35.034、9.645,P值分别为0.000、0.002;胃癌组Hp感染率高于癌前病变组,χ2=7.221,P=0.007。Maspin蛋白表达在浅表性胃炎、癌前病变及胃癌中阳性率分别是58.5%(38/65)、82.8%(48/58)和32.9%(26/79),浅表性胃炎和癌前病变组maspin表达均高于胃癌组,χ2值分别为9.428、33.457,P值分别为0.002、0.000;癌前病变组织中maspin表达高于浅表性胃炎,χ2=8.603,P=0.003。在浅表性胃炎、癌前病变及胃癌组织中,Hp感染阳性组maspin表达阳性率均较Hp感染阴性组低,且差异有统计学意义,χ2值分别为6.548、26.619和4.950,P值分别为0.010、0.000和0.029。胃癌组织中maspin蛋白的表达与肿瘤分化程度、周围组织浸润及淋巴结是否发生转移显著相关,P值分别为0.017、0.033和0.006。结论:Hp感染在胃黏膜演变过程中起着重要作用,Hp感染可能通过使maspin基因失活从而诱发胃黏膜的癌变,maspin蛋白的表达失活可能是Hp致癌的作用机制之一。     

幽门螺杆菌与胃癌相关性研究

（目的）研究幽门螺杆菌（Ｈｐ）与胃癌发生之间的关系。（方法）用美蓝染色对７４１例胃炎性病变和１３１例胃癌病人之胃粘膜活检组织的Ｈｐ感染情况进行检测。（结果）胃癌组和慢性萎缩性胃炎组（ＣＡＧ）Ｈｐ检出率分别为６２．５９％和６１．６０％,明显高于慢性浅表性胃炎组（ＣＳＧ）的３８．６１％（Ｐ〈０．０１）。胃癌组中,伴有癌周粘膜肠化生者Ｈｐ检出率明显高于不伴肠化生才（Ｐ〈０．０５）,在活动性ＣＳＧ和ＣＡＧ     

幽门螺杆菌与胃癌相关性研究

［目的］研究幽门螺杆菌（Ｈｐ）与胃癌发生之间的关系。［方法］用美蓝染色对７４１例胃炎性病变和１３１例胃癌病人之胃粘膜活检组织的Ｈｐ感染情况进行检测。［结果］胃癌组和慢性萎缩性胃炎组（ＣＡＧ）Ｈｐ检出率分别为６２．５９％和６１．６０％,明显高于慢性浅表性胃炎组（ＣＳＧ）的３８．６１％（Ｐ＜０．０１）;胃癌组中,伴有癌周粘膜肠化生者Ｈｐ检出率明显高于不伴肠化生者（Ｐ＜０．０５）;在活动性ＣＳＧ和ＣＡＧ中,Ｈｐ检出率分别为８９．４１％和９０．５３％,而在非活动性ＣＳＧ和ＣＡＧ中仅分别为１．７１％和１．２３％,两者差异非常显著（Ｐ＜０．０１）。［结论］提示Ｈｐ感染与胃癌的发生有显著的相关性;Ｈｐ有可能通过引发活动性胃炎、腺体萎缩、上皮肠化生等方式参与胃癌的发生。     

卵巢癌顺铂耐药分子生物学研究进展

 化疗耐药是有效治疗卵巢癌的重大障碍。卵巢癌耐药是多因素、多因子共同作用的结果,耐药相关基因的深入研究为从根本上逆转肿瘤耐药提供了新的思路。     

幽门螺杆菌与残胃癌

残胃癌发病与幽门螺杆菌感染密切相关,幽门螺杆菌能促进残胃黏膜上皮细胞增殖,促进胃液中亚硝基化合物的产生及人体某些基因异常表达,最终促使残胃癌发生.根除幽门螺杆菌感染有望减少残胃癌的发生.     

幽门螺杆菌感染、细胞凋亡与胃癌相关性研究进展

幽门螺杆菌与胃癌发生及细胞凋亡与胃癌发生发展的关系是近年来胃癌机制研究中的两大热点。最近研究提示幽门螺杆菌可能通过细菌凋亡途径致癌。现就三者间的相互关系作一综述。     

幽门螺杆菌感染及其相关因素与胃癌关系的研究进展

 胃癌是人类最常见的恶性肿瘤之一,目前研究认为幽门螺杆菌（HP）是胃癌发生发展进程的重要推动因素,现就目前国内外学者对HP在胃癌发生中致病的毒力因子及作用机制、宿主基因的易感性和环境因素三个方面进行综述。     

幽门螺杆菌感染与结直肠癌相关性的研究

目的:探讨幽门螺杆菌(Helicobacter pylori,Hp)感染与结直肠癌的相关性.方法:分析2015年6月至2020年6月郑州大学第一附属医院诊治的70例结直肠癌患者,选取同期于本院体检的99例健康体检者为对照组,应用13C尿素呼气试验检测结直肠癌组与对照组的Hp感染率.结果:对照组Hp阳性51例,阳性率51...     

Epidemiology of Helicobacter pylori and gastric cancer

Findings in epidemiological studies of the relationship between Helicobacter pylori and gastric cancer have been inconsistent: many studies have yielded a positive relationship, whereas several studies have shown no relationship. The inconsistency arises because of the occurrence of seroreversion during the period between the time that H. pylori exerts a carcinogenic effect and the time of blood sampling. When this seroreversion is taken into account, there is an epidemiologically positive association between H. pylori status and the risk for gastric cancer. In addition to the epidemiological evidence, experimental studies using Mongolian gerbils have shown that H. pylori infection elevates the risk for gastric cancer. It is concluded that H. pylori is a causal factor for gastric cancer. In the creation of preventive strategies against gastric cancer by the eradication of H. pylori, determination of the time at which H. pylori plays a role as a carcinogen is important. Three hypotheses have been proposed in regard to this timing: that H. pylori infection in childhood or the teenage years acts as a factor that produces precancerous lesions with irreversible damage in the gastric mucosa, that in adulthood it acts as an initiator, and also in adulthood, that it acts as a promoter. As these hypotheses are not mutually exclusive, the extent to which each hypothesis plays a part in explaining gastric carcinogenesis should be evaluated. Only a small proportion of subjects infected with H. pylori have gastric cancer during their lifetime. Interleukin-1 polymorphism, a host factor, and CagA, a virulence factor of H. pylori, are suspected to be risk factors for gastric cancer in subjects with H. pylori infection. Dietary factors, especially vitamin C, and patterns of precancerous lesions also seem to influence the relationship between H. pylori and gastric cancer. H. pylori seems to reduce the risk for esophageal and for some gastric cardia adenocarcinomas. This finding, as well as determination of the time at which H. pylori exerts this preventive effect, should be considered in the creation of preventive strategies against gastric cancer that target the eradication of H. pylori. Received: June 1, 2001 / Accepted: October 16, 2001     

幽门螺杆菌对胃癌hMLH1和hMSH2基因表达的影响

目的探讨幽门螺杆菌(Hp)对胃癌中hMLH1和hMSH2基因表达的影响和Hp的致癌机制.方法利用免疫组织化学S-P法检测胃癌、癌旁和胃炎黏膜中hMLH1、hMSH2 基因的表达情况.结果在全部被检组织中,Hp感染组hMLH1和hMSH2表达阳性率均低于相应的非感染组,其中胃癌组织中hMSH2表达阳性率在Hp感染组(54.7%)和非感染组(82.1%)差异有显著性(P<0.05).结论 Hp感染引起hMLH1和hMSH2基因表达降低,这可能是Hp导致胃癌的分子机制之一.     

Helicobacter pylori but not gastrin is associated with the development of colonic neoplasms

Recent studies have suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of colonic neoplasia. Hypergastrinemia can be induced by H. pylori infection, and gastrin can act as putative promoter of colorectal carcinogenesis. Aim of our study was to assess whether H. pylori infection and/or increased serum gastrin levels are associated with the occurrence of colonic neoplasms. For this, we reviewed prospectively collected data of 377 patients with a minimum age of 50 years who underwent colonoscopy. H. pylori and CagA status were determined by serology. Serum gastrin levels were measured in fasting state by commercially available assay. In H. pylori infected patients (n = 138; 36.6%), the overall prevalence of colonic neoplasms was more frequent compared to H. pylori negative patients (n = 239; 63.4%) (OR = 2.73, 95% CI: 1.76–4.24). H. pylori infection occurred more frequently in patients with hyperplastic polyps (OR = 2.66, 95% CI: 1.23–5.74) and adenomas presenting with low grade intraepithelial neoplasia (IEN) (OR = 1.85, 95% CI: 1.14–2.99). Attributable risk for adenomas with high grade IEN and colorectal adenocarcinoma (n = 14) was not assessed due to the low number of cases. The expression of CagA was also associated with an increased risk for colonic neoplasms (OR = 2.25, 95% CI: 1.29–3.94). Hypergastrinemia did not increase the risk for any colonic neoplasms and there was no difference in basal serum gastrin levels between H. pylori positive and negative patients. In conclusion, H. pylori infection, including CagA expression is associated with an increased risk for the development of colonic neoplasm.     

胃癌组织中H.pylori感染与bFGF蛋白表达关系及其临床意义

目的 :探讨幽门螺旋杆菌感染(Helicobacterpylori,H .pylori)与碱性成纤维细胞生长因子 (basicfibroblastgrowthfac tor ,bFGF)蛋白表达的关系及其与胃癌发生和发展的关系。方法 :应用免疫组化方法检测了 63例胃癌存档标本和 10例正常胃组织中bFGF的蛋白表达。结果 :63例胃癌存档蜡块中有 45例阳性 ,Hp阳性胃癌组和转移性胃癌组显著高于Hp阴性胃癌组和非转移性胃癌组 ,P <0 0 1。阳性着色定位于肿瘤细胞、血管内皮细胞及肿瘤基质。结论 :H .pylori感染增强了bFGF的表达 ,bFGF可能通过自分泌和旁分泌机制诱导胃癌血管生成 ,或通过胞内分泌作用刺激某些酶的产生 ,从而促进肿瘤的浸润。     

Hp感染与胃癌中癌基因和抑癌基因蛋白表达的关系

目的研究Hp感染与胃癌发生的关系及其可能的致癌机制。方法经内镜和病理诊断的胃癌91例,用快速尿素酶试验,改良W-S银染色和PCR方法检测上述标本中Hp;以S-P免疫组织化学法检测P21、P53、C-mcy及C-erbB-2,并用阳性表达积分半定量和免疫组化图像分析进行比较。结果Hp阳性胃癌组(44例)的P21、P53、C-myc及C-erbB-2表达阳性率较Hp阴性胃癌组(47例)为高。Hp阳性组这4种癌基因蛋白的阳性表达积分、平均光密度和积分光密度均显著高于Hp阴性组(P<0.05～0.01)。结论Hp感染与胃癌中P21、P53、C-myc及C-erbB-2的异常表达密切相关,提示Hp感染可使胃粘膜细胞的癌基因活化和抑癌基因突变或失活,促进胃粘膜细胞恶性转化而导致胃癌发生。