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(Helicobacter pylori．H．pylori)与碱性成纤维细胞生长因子(basic fibroblast growth factor．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<0．01。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。     

胃癌组织中肥大细胞与C-erbB-2癌基因蛋白

 用俾士麦棕法和免疫组织化学方法检测了57例胃癌组织中肥大细胞(MC)和C-erbB-2癌基因蛋白。 结果表明:(1)MC计数与胃癌的分化程度和转移有关, 高、中分化腺癌高于低分化腺癌和未分化癌(P＞0.05), 无转移者高于有转移者(P＞0.05); (2)C-erbB-2癌基因蛋白阳性表达与胃癌的分化程度和转移无关(P＞0.05); (3)C-erbB-2癌基因蛋白阳性表达与MC计数有关, MC高计组, C-erbB-2癌基因蛋白阳性表达低于MC低计组(P＞0.05)。     

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。     

Survivin蛋白在胃癌组织中的表达及其与Hp感染的关系

目的 探讨胃癌组织中Survivin蛋白的表达及其与幽门螺杆菌(Hp)感染的关系.方法 采用免疫组化S-P法检测64例胃癌组织中Survivin蛋白的表达情况;采用快速尿素酶试验及Warthin-starry银染色法检测64例胃癌组织的Hp感染情况.结果 64例胃癌组织中Survivin蛋白的阳性率为50.0%;Ⅲ～Ⅳ期胃癌组织Survivin蛋白的阳性率高于I～Ⅱ期胃癌组织,有淋巴结转移胃癌组织Survivin蛋白的阳性率高于无淋巴结转移胃癌组织,Hp阳性胃癌组织中Survivin蛋白的阳性率高于Hp阴性胃癌组织,差异均有统计学意义(P<0.05).结论 Survivin蛋白的表达可能与胃癌的发展、生物学行为和预后有关,Hp感染能够促进其表达.     

胃癌中RUNX3蛋白表达与胃癌关系的研究

背景与目的:探讨RUNX3基因表达与胃癌发生发展和转移的关系。材料与方法:采用羊抗人RUNX3蛋白抗体和枸橼酸_微波_SP免疫组织化学方法检测胃癌标本和正常胃组织阳性细胞数及阳性率,并采用Westernblot检测胃癌中RUNX3蛋白的表达状况。结果:免疫组化结果表明RUNX3在正常胃组织中阳性率100%,在胃癌中阳性率为51.13%,两者间的差异具有统计学意义(P<0.05);RUNX3蛋白的丢失在胃癌中占48.87%,并且与胃癌的组织类型、淋巴结转移状况有关。Westernblot结果表明RUNX3在胃癌组织中表达明显低于相应正常胃组织,且高分化胃癌中RUNX3蛋白表达高于低分化胃癌。结论:RUNX3可能是胃癌发生中重要的候选抑癌基因。     

Hp感染与胃癌组织中Bcl-2、Bax表达的相关性研究

目的 揭示Bcl-2,Bax在胃癌组织的表达与Hp感染的相关性.方法 采用快速尿素酶试验及组织学改良Giemsa染色法联合检测130例胃癌组织与70例慢性胃炎组织中Hp感染情况,免疫组织化学PV9000法,检测130例胃癌组织与70例慢性胃炎组织中Bcl-2,Bax蛋白的阳性表达情况.结果 Hp(+)组Bcl-2蛋白的阳性表达率明显高于Hp(-)组(P<0.01);胃癌组织中Hp感染与Bcl-2蛋白表达之间存在正相关关系(P<0.01,r=0.288);Hp(+)组Bax蛋白的阳性表达率明显低于Hp(-)组(P<0.01);胃癌组织中Hp感染与Bax蛋白表达之间存在负相关关系(P<0.01,r=-0.536).结论 Hp感染与Bcl-2蛋白表达存在正相关性,与Bax蛋白表达存在负相关性,提示Hp感染与细胞凋亡,二者可能共同参与胃癌的发生发展过程.     

Hp感染与胃癌组织中Bcl-2、Bax表达的相关性研究

目的：揭示Bcl-2,Bax在胃癌组织的表达与Hp感染的相关性。方法：采用快速尿素酶试验及组织学改良Giemsa染色法联合检测130例胃癌组织与70例慢性胃炎组织中Hp感染情况,免疫组织化学PV9000法,检测130例胃癌组织与70例慢性胃炎组织中Bcl-2,Bax蛋白的阳性表达情况。结果：Hp（＋）组Bcl-2蛋白的阳性表达率明显高于Hp（-）组（P〈0.01）;胃癌组织中Hp感染与Bcl-2蛋白表达之间存在正相关关系（P〈0.01,r=0.288）;Hp（＋）组Bax蛋白的阳性表达率明显低于Hp（-）组（P〈0.01）;胃癌组织中Hp感染与Bax蛋白表达之间存在负相关关系（P〈0.01,r=-0.536）。结论：Hp感染与Bcl-2蛋白表达存在正相关性,与Bax蛋白表达存在负相关性,提示Hp感染与细胞凋亡,二者可能共同参与胃癌的发生发展过程。     

Hp感染与胃癌组织HIF-1α表达相关性及生物学意义的研究

目的:探讨胃癌组织HIF-1α的表达与幽门螺杆菌(Hp)感染的相关性,以及两者与胃癌临床病理特征之间的关系。方法:采用快速尿素酶试验和组织学改良Giemsa染色法联合检测130例胃癌组织与70例慢性胃炎组织中Hp感染情况,采用免疫组织化学PV9000法,检测130例胃癌组织与70例慢性胃炎组织中HIF-1α蛋白的阳性表达情况。结果:胃癌组明确感染Hp的患者有100例,Hp阳性感染率为72.0%,明显高于胃炎组的46.0%,χ2=9.703,P<0.01;胃癌组HIF-1α蛋白阳性表达率为56.0%,明显高于胃炎组的14.0%,χ2=24.138,P<0.01;Hp(+)组HIF-1α蛋白的阳性表达率为63.9%,明显高于Hp(-)组的35.7%,χ2=6.495,P<0.05;胃癌组织中Hp感染与HIF-1α蛋白表达之间存在正相关,r=0.255,P<0.05;Hp感染与胃癌组织浸润深度及有无淋巴结转移有关,P值均<0.05,而与组织分化程度无关,P>0.05。HIF-1α蛋白的表达水平与胃癌组织浸润深度(P<0.05)及有无淋巴结转移(P<0.01)有关,而与组织分化程度无关,P>0.05。结论:Hp感染与HIF-1α蛋白表达可能在胃癌的发生中起协同作用,并与胃癌的浸润深度及淋巴结转移等密切相关。     

胃癌组织中抑癌及相关基因的表达及其临床意义

目的探讨胃癌组织中抑癌基因nm23和E-cadherin及肿瘤相关基因CD44s表达及与其临床病理特征的关系。方法应用免疫组化SP法,检测50例胃癌组织及其癌旁组织中nm23和E-cadherin及CD44s基因的表达,应用统计学方法分析与其临床病理特征的相关性。结果胃癌组织中nm23和E-cadherin及CD44s基因阳性表达率分别为48.0%和44.5%及52.0%。nm23和E-cadherin基因阳性表达率与胃癌组织学分化程度、临床分期和淋巴结转移等密切相关,P均〈0.05。CD44s阳性表达与肿瘤是否有浆膜浸润、淋巴结转移和TNM分期相关,P〈0.05。CD44s表达与nm23表达呈一定程度的负相关性,nm23表达与E-cadherin表达呈正相关性。结论 nm23和E-cadherin及CD44s基因与胃癌的发生和转移相关,检测其表达可预测胃癌转移和侵袭程度。     

胃黏膜癌前病变和胃癌组织相关癌基因和抑癌基因表达差异的研究

目的:探讨胃黏膜癌前病变与胃癌组织中Bcl-2、Bax、p16和p53蛋白的表达和意义。方法:用免疫组化法检测Bcl-2、Bax、p16和p53产物在79例胃癌、23例胃黏膜不典型增生和21例肠上皮化生组织中的表达。结果:Bcl-2在胃癌和不典型增生组织中的阳性率分别为73.4%(58/79)和78.2%(18/23),差异无统计学意义,P=0.273;但是显著高于肠上皮化生组织(38.1%,8/21),P<0.01。Bax、p16和p53在胃癌和不典型增生及肠上皮化生组织中的阳性率分别为41.8%(31/79)、69.6%(18/23)、80.9%(17/21)和45.6%(36/79)、65.2%(15/23)、76.1%(16/21)及82.3%(65/79)、39.1%(9/23)、28.6%(6/21),差异有统计学意义,P<0.01。结论:Bcl-2对胃黏膜细胞凋亡有明显的负性调节作用,而抑癌基因Bax表达对Bcl-2的抑制凋亡功能有对抗调节作用;p16基因直接参与细胞生长增殖的负调节,突变的p53基因通过抑制细胞凋亡而参与胃癌的发生。     

胃癌及其有关病变的幽门螺杆菌感染与抑癌基因表达的相关性研究

背景与目的:幽门螺杆菌(Helicobacterpylori,Hp)是确定的胃癌致癌因子,但其致癌的确切机制仍不清楚。p53、p21WAF1、p16为主要的细胞周期负调控基因。本研究旨在探讨胃癌及其有关病变中,上述3种抑癌基因的作用及其与幽门螺杆菌感染的关系。方法:应用HID-AB(pH2.5)-PAS、SP免疫组化染色及Warthin-Starry染色,对65例慢性萎缩性胃炎(chronicatrophicgastritis,CAG),93例肠上皮化生(intestinalmetaplasia,IM),94例胃上皮不典型增生(gastricepithelialdysplasia,GED)及60例胃癌(gastriccarcinoma,GC)中3种抑癌基因表达和幽门螺杆菌感染情况进行检测。结果:在胃癌发生的不同阶段,p53阳性表达率随病变发展而升高,在CAG、IMⅠ～Ⅱ、IMⅢ、GEDⅠ级、GEDⅡ～Ⅲ级及GC中分别为0、1.64%、6.25%、5.45%、23.08%、70.00%。p21WAF1和p16阳性表达率随病变发展而降低,p21WAF1阳性表达率分别为100%、95.08%、100%、100%、71.79%、45.00%,p16阳性表达率分别为83.08%、81.97%、78.13%、89.09%、69.23%、40.00%。三者表达在GEDⅡ～Ⅲ与GEDⅠ组间、GC与GEDⅡ～Ⅲ组间的差异均具有显著性(P<0.05)。同一病变中,Hp感染阳性组p53、p21WAF1及p16阳性表达率虽然高于Hp阴性组,但差异无显著性(P>0.05)。结论:p53突变及p21WAF1、p16失活     

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...     

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。     

CagA+ Helicobacter pylori infection and gastric cancer risk in the EPIC-EURGAST study

Helicobacter pylori (H. pylori), atrophic gastritis, dietary and life-style factors have been associated with gastric cancer (GC). These factors have been evaluated in a large case-control study nested in the European Prospective Investigation into Cancer and Nutrition carried out in 9 countries, including the Mediterranean area. Participants, enrolled in 1992-1998, provided life-style and dietary information and a blood sample (360,000; mean follow-up: 6.1 years). For 233 GC cases diagnosed after enrolment and their 910 controls individually-matched by center, gender, age and blood donation date H. pylori antibodies (antilysate and antiCagA) and plasma Pepsinogen A (PGA) were measured by ELISA methods. Severe chronic atrophic gastritis (SCAG) was defined as PGA circulating levels <22 microg/l. Overall, in a conditional logistic regression analysis adjusted for education, smoke, weight and consumption of total vegetables, fruit, red and preserved meat, H. pylori seropositivity was associated with GC risk. Subjects showing only antibodies anti-H. pylori lysate, however, were not at increased risk, while those with antiCagA antibodies had a 3.4-fold increased risk. Overall, the odds ratio associated with SCAG was 3.3 (95% CI 2.2-5.2). According to site, the risk of noncardia GC associated with CagA seropositivity showed a further increase (OR 6.5; 95% CI 3.3-12.6); on the other hand, a ten-fold increased risk of cardia GC was associated with SCAG (OR 11.0; 95% CI 3.0-40.9). These results support the causal relationship between H. pylori CagA+ strains infection, and GC in these European populations even after taking into account dietary habits. This association was limited to distal GC, while serologically defined SCAG was strongly associated with cardia GC, thus suggesting a divergent risk pattern for these 2 sites.     

幽门螺杆菌与大肠癌相关性研究进展

幽门螺杆菌(Hp)感染与大肠癌之间关系的研究发现,大肠癌及其相关腺瘤患者的Hp感染率较高,提示Hp有可能通过自身毒力和升高血浆胃泌素水平等方式作用于局部和远处的大肠黏膜细胞致癌,Hp感染是大肠癌的一种潜在危险因素.     

Association between C1019T polymorphism in the connexin 37 gene and Helicobacter pylori infection in patients with gastric cancer

Objective: To investigate the association between the connexin 37 C1019T polymorphism and Helicobacterpylori infection in patients with gastric cancer. Methods: 388 patients with gastric cancer (GC), 204 with chronicsuperficial gastritis (CSG) were studied. H. pylori was detected by gastric mucosal biopsies biopsy dyeing method.Connexin 37 gene polymorphism 1019 site genotypes were determined by gene sequencing technology. Genotypesand alleles frequencies were compared. Results: (1) Connexin37 gene 1019 site distribution frequency (CC type,TC type, TT type) in the CSG group was 18.1%, 45.1% and 36.8%; in the stomach cancer group it was 35.1%,45.9% and 19.%, conforming to the Hardy-Weinberg euilibrium. (2) In comparison with CSG group, thefrequency of Connexin37 C allele was higher in the gastric cancer group (58.0% vs 40.7%, OR = 2.01, 95%CI =1.58-2.57, P < 0.01). The prevalence of gastric cancer risk was significantly increased in the carriers of C allele(CC+TC) than in TT homozygote (OR = 2.47, 5%CI = 1.68- 3.610. (3) Gastric cancer patients complicated withHp infection 211 cases, gastric cancer group of the male patients with HP positive patients with 187 cases, 40cases of female patients with negative patients, 24 cases were HP positive, negative in 137 cases, control groupmale patients, 28 cases were Hp positive, negative in 95 patients, female patients with Hp positive 6 cases, 75cases were negative. On hierarchical analysis, the male group OR value was 15.9 (95%CI to 9.22-27.3), and thefemale OR was 2.19 (95%CI 0.88-5.59), indicating a greater contribution in males (P <0.01). After eliminationof gender effects, positive HP and gastric cancer were closely related (OR 8.82, 95% CI: 5.45-14.3). (4) Thedistribution frequency of C allele in patients with Hp infection was much higher than that in Hp negative casesin the GC group (64.5% vs 47.0%, OR = 2.05, 95%CI = 1.54-2.74, P < 0.01). Compared with TT homozygotes,(CC+TC) genotype prevalence of gastric cancer risk increased significantly (OR = 2.96, 5%CI = 1.76-2.99 ).Conclusion: The T allele in the connexin37 gene might not only be associated with gastric cancer but also withH. pylori infection.     

Helicobacter pylori,gastric microbiota and gastric cancer relationship: Unrolling the tangle

Helicobacter pylori infection (Hp-I) represents a typical microbial agent intervening in the complex mechanisms of gastric homeostasis by disturbing the balance between the host gastric microbiota and mucosa-related factors, leading to inflammatory changes, dysbiosis and eventually gastric cancer. The normal gastric microbiota shows diversity, with Proteobacteria [Helicobacter pylori (H. pylori) belongs to this family], Firmicutes, Actinobacteria, Bacteroides and Fusobacteria being the most abundant phyla. Most studies indicate that H. pylori has inhibitory effects on the colonization of other bacteria, harboring a lower diversity of them in the stomach. When comparing the healthy with the diseased stomach, there is a change in the composition of the gastric microbiome with increasing abundance of H. pylori (where present) in the gastritis stage, while as the gastric carcinogenesis cascade progresses to gastric cancer, the oral and intestinal-type pathogenic microbial strains predominate. Hp-I creates a premalignant environment of atrophy and intestinal metaplasia and the subsequent alteration in gastric microbiota seems to play a crucial role in gastric tumorigenesis itself. Successful H. pylori eradication is suggested to restore gastric microbiota, at least in primary stages. It is more than clear that Hp-I, gastric microbiota and gastric cancer constitute a challenging tangle and the strong interaction between them makes it difficult to unroll. Future studies are considered of crucial importance to test the complex interaction on the modulation of the gastric microbiota by H. pylori as well as on the relationships between the gastric microbiota and gastric carcinogenesis.