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。     

膀胱癌组织中bFGF蛋白的表达及其临床意义

目的 :探讨碱性成纤维细胞生长因子 (bFGF)与膀胱癌发生发展的关系。方法 :应用免疫组化方法检测了 4 8例膀胱癌存档标本和 4例正常膀胱组织中bFGF的蛋白表达。结果 :4 8例膀胱癌存档蜡块中有 2 3例阳性 ,浸润性癌显著高于浅表癌 (P <0 .0 1) ,除G1和G2 之间外各分级阳性率之间差异也有显著性。阳性着色定位于肿瘤细胞、血管内皮细胞、正常逼尿肌及肿瘤基质。结论 :bFGF可能通过自分泌和旁分泌机制诱导膀胱癌血管生成 ,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。bFGF高表达对预测膀胱癌患者的复发和预后有一定的指导意义。拮抗bFGF的作用可能是治疗和预防膀胱癌复发和转移的一条新途径。     

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.     

利用组织芯片技术观察Hp感染与p53、p63表达在胃癌中的相关性

目的:研究Hp与p53、p63表达与胃癌临床病理特征的关系。方法:应用免疫组化技术检测人胃癌组织芯片144芯中Hp、p53和p63的表达。结果:144例胃癌标本中p53阳性表达80例（55.6%）,p63阳性表达53例（36.8%）,Hp阳性表达94例（65.3%）。p53表达与胃癌组织学分型、病理分级和淋巴结转移有关(P＜0.05),与肿瘤部位及浸润深度无关(P＞0.05);p63在低分化腺癌组织中表达率明显高于高、中分化腺癌(P＜0.05),与肿瘤部位、浸润深度及淋巴结转移无关(P＞0.05);Hp主要寄居在胃窦,且其感染与肿瘤组织学分型和病理分级有关(P＜0.05),与淋巴结转移及浸润深度无关(P＞0.05)。胃癌组织中Hp感染与p53表达呈正相关(r=0.20,P＜0.05)。结论:p53和p63的高表达与胃癌的发生及进展密切相关,但p53和p63在胃腺癌发生发展过程中并无交互作用, Hp感染与p53高表达存在一定相关性。     

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。     

根治幽门螺杆菌对胃粘膜上皮p53蛋白表达的影响

目的　研究幽门螺杆菌 (Hp)根除治疗对p5 3蛋白表达的影响 ,探讨Hp与胃癌的关系。 方法　利用免疫组化染色对 2 0 6例胃粘膜活检组织 ,包括正常胃粘膜、Hp阴性胃癌前各阶段病变、Hp阳性胃癌前各阶段病变Hp根除治疗前后及胃癌 ,进行 p5 3蛋白表达的分析。 结果　正常胃粘膜未见 p5 3蛋白表达。Hp阳性胃癌前阶段病变 p5 3蛋白表达阳性率显著高于正常胃粘膜及Hp阴性胃癌前阶段病变 ,其中Hp阳性肠上皮化生 p5 3蛋白表达阳性率显著高于Hp阴性相应病变组 ,低于Hp阳性异型增生组。Hp阳性胃癌前阶段病变Hp根除治疗后 ,其 p5 3蛋白表达阳性率显著降低。结论　Hp根除治疗后 ,胃癌前阶段病变p5 3蛋白表达阳性率明显降低 ;Hp感染可促进突变型 p5 3基因表达增强。     

胃癌高危人群胃黏膜组织中Runx3蛋白表达与Hp感染研究的关系

目的：对胃癌高危人群胃黏膜组织中的Runx3蛋白及Hp进行检测，探讨Runx3蛋白与Hp感染在陕北胃癌高发的关系。方法：免疫组化法（S—P）检测178例胃癌高危人群胃黏膜活检标本（其中1例为胃癌）和63例胃癌（GC）组织标本中Runx3蛋白的表达情况，HE染色和特殊染色检测Hp感染情况。结果：178例胃黏膜组织中，Runx3蛋白在102例慢性浅表性胃炎（CSG）中的阳性表达率为81．37％，在76例慢性萎缩性胃炎（CAG）中的阳性表达率为72．37％，在伴有肠上皮化生（IM）的60例中阳性率为61．67％，在伴有异型增生（DYS）的9例中阳性表达率为55．55％，63例GC中的阳性表达率为41．26％。GC与CSG中的阳性表达率相比有显著性差异（P〈0．005），Gc与CAG中的阳性表达率相比有显著性差异（P〈0．005），Gc与伴IM中的阳性表达率相比有统计学意义（P〈0．05），Gc与伴DYS中的阳性表达率相比无统计学意义（P〉0．05）。Hp在CSG中的感染率为40．19％，在CAG中的感染率为65．78％，在伴IM中的感染率为66．67％，在伴DYS中的感染率为77．78％，随着病变的进展Hp的感染率有逐渐升高的趋势，（P〈0．005）。91例Hp阳性组中Runx3蛋白的阳性表达率为54．94％，87例Hp阴性组中Runx3蛋白的阳性表达率为78．16％，二者有显著性差异（P〈0．005）。结论：Runx3基因和Hp感染是胃癌高发的重要因素，可能有协同致癌作用。     

胃癌组织幽门螺杆菌感染与EB病毒潜伏膜蛋白表达的相关性

目的:观察胃癌组织中幽门螺杆菌(H.pylori)感染和EB病毒潜伏膜蛋白(EBV-LMP)的同步表达情况,探讨两者在胃癌中的相互关系.方法:80例正常胃黏膜组织和97例胃癌组织,利用HE染色对所取标本进行组织病理学诊断,EBV-LMP测定采用免疫组化SP法,H.pylori感染判定采用HE,H.pylori-DNAPCR和血清ELISA法测定IgG抗体三种方法.结果:正常胃黏膜组织未见EBV-LMP的表达,胃癌黏膜组织EBV-LMP表达阳性率为7.2%(7/97),胃癌组织EBV-LMP表达明显高于正常胃黏膜组织,差异有统计学意义(P＜0.05).本组病例中H.pylofi感染的胃癌黏膜组织中EBV-LMP的阳性表达率为13.5%(7/52),无H.pylori感染的胃癌组织EBV-LMP的阳性表达率为0,H.pylori感染的胃癌组织EBV-LMP表达明显高于无H.pylori感染的胃癌组织,差异有统计学意义(P＜0.05).结论:正常胃黏膜组织无EBV-LMP的表达,胃癌组织中EBV-LMP表达明显高于正常胃黏膜组织,H.pylori感染胃癌组织比无H.pylori感染胃癌组织EBV-LMP呈现高表达,H.pylori感染和EB病毒感染在胃癌的发生和发展过程中可能具有更加深在的相互关系.     

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。     

胃癌中幽门螺杆菌对hMSH2和hMLH1基因表达的影响

目的：探讨胃癌中幽门螺杆菌（Helicobacter pylori，Hpylori）对hMSH2和hMLH1基因表达的影响，方法：利用尿素酶快速检验法确定胃癌组织及同病例癌旁粘膜、胃镜非癌患者胃粘膜组织有无Hpylori感染；应用免疫组织化学方法检测所有标本的hMSH2、hMLH1蛋白的表达。结果：胃癌组的hMSH2蛋白阳性表达率显著高于癌旁组和非癌组（P〈0．05）；而后两者无显著差别（P〉0．05）。胃癌组、癌旁组和非癌组的hMLH1蛋白阳性表达率无显著差别（P〉0．05）。胃癌组织中，Hpylori感染组的hMSH2蛋白阳性表达率和hMLH1蛋白阳性表达率均显著低于非感染组（P〈0．05）；癌旁组织中．Hpylori感染组的hMSH2蛋白阳性表达率和hMLH1蛋白阳性表达率均显著低于非感染组（P〈0．05）；非癌患者胃粘膜中，H pylori感染组与非感染组的hMSH2蛋白阳性表达率及hMLH1蛋白阳性表达率均无显著差别（P〉0．05）。结论：胃粘膜hMSH2蛋白表达上调并hMLH1蛋白表达下调可能是胃癌发生的标志；Hpylori感染导致的胃粘膜细胞hMSH2和hMLH1蛋白表达降低，可能是促进胃癌发生的一个因素.     

Sirt1 Gene Expression and Gastric Epithelial Cells Tumor Stage in Patients with Helicobacter pylori Infection

Introduction: The World Health Organization has categorized Helicobacter pylori as a carcinogen for gastriccancer, which causes human mortality worldwide. A number of studies have shown that H. pylori affects cell signalingin gastric epithelial cells and changes the expression of some proteins such as proinflammatory cytokines. Bacterialinfections may alter sirt1 and sirt2 genes expression in inflammatory tissues and cancer cells. In this study, sirt1 andsirt2 genes expression in gastric cancers was surveyed with reference to H. pylori status. Methods: Stomach biopsieswere collected from 50 gastric cancer patients, 25 H. pylori-positive and 25 H. pylori-negative as determined by theurea rapid test. Tumor grade was determined by a pathologist. After total RNA extraction from gastric cancer biopsysamples and cDNA synthesis, sirt1 and sirt2 genes expression levels were determined by Real Time PCR and ΔΔCTmethods. Results: There was no statistically significant link between H. pylori infection and sirt1 (P<0.899) and sirt2(P<0.169) genes expression in gastric epithelial cells. However, pathologic findings showed that there is a statisticallysignificant relationship between sirt1 gene expression and the tumor grade (P<0.024). Discussion: A statisticallysignificant association was found between sirt1 gene expression and tumor grade of gastric cancers that could be dueto effects on progression of cancer cells infected with H. pylori.     

HLA-G Expression in Tumor Tissues and Soluble HLA-G Plasma Levels in Patients with Gastrointestinal Cancer

Background: Overexpression of human leukocyte antigen G (HLA-G) and increased plasma levels of solubleHLA-G (sHLA-G) have been reported in different human malignancies, and are believed to be involved in tumor immuneevasion. Objectives: This study was designed to evaluate the expression of HLA-G in tumor tissues and the plasmalevels of sHLA-G in patients with gastrointestinal cancer, and to determine their associations with clinicopathologicalfactors. The link between Helicobacter pylori infection and increased HLA-G expression or sHLA-G levels was alsoinvestigated in patients with gastric cancer. Methods: HLA-G expression was investigated in tumor tissues from 100patients with gastric and colorectal adenocarcinoma using immunohistochemistry test, and plasma levels of sHLA-Gwere measured in 82 patients with ELISA method. The presence of H. pylori genome was investigated in tumortissues from 25 patients with gastric cancer by PCR method. Results: HLA-G expression was observed in 43% ofcolorectal cancers and 34.6% of gastric cancers, and was not related with any of the clinicopathological factors. Therewas a significant correlation between increased sHLA-G level and stage I tumors. Eight of 25 (32%) gastric cancerspecimens were positive for H. pylori, of which 3 samples were positive for HLA-G. Soluble HLA-G levels were abovethe cut-off value in all H. pylori-positive patients. Conclusion: Plasma levels of sHLA-G were significantly increasedin our patients with a sensitivity of 89% and a specificity of 62%. Soluble HLA-G level can be considered a usefulindicator for the early diagnosis of gastric and colorectal adenocarcinoma.     

Expression of cyclooxygenase-2 in primary and remnant gastric carcinoma: comparing it with p53 accumulation,Helicobacter pylori infection,and vascular endothelial growth factor expression

BACKGROUND AND OBJECTIVES: Cyclooxygenase-2 (COX-2) expression may contribute to the synthesis of prostanoids, which have been related to carcinogenesis and tumor progression. It is well known that the gastric remnant is at greater risk of the development of gastric cancer than is the whole stomach; incidence rates for gastric cardia adenocarcinoma are rising in the United States and Europe. Our objective was to determine the involvement of COX-2 in primary and remnant gastric cancer tissues as well as in adjacent noncancerous mucosa. METHODS: We investigated the expression of COX-2 in 91 human gastric cancer tissue and adjacent noncancerous mucosa samples (40 remnant gastric cancer, 37 gastric cardia cancer, and 14 gastric corpus and antrum cancer), using immunohistochemistry. In addition, p53 expression, Helicobacter pylori infection, and vascular endothelial growth factor in the tissues were evaluated by immunohistochemical staining and compared with COX-2 expression. RESULTS: There were no significant differences in clinicopathological data in the gastric cancer tissues. There was a significant relation between the expression of COX-2 and p53 in gastric cancer tissues (P = 0.0048). However, vascular endothelial growth factor expression and Helicobacter pylori infection showed no correlation with the expression of COX-2. In the case of adjacent noncancerous mucosa, the positive rate of COX-2 expression was significantly higher in the remnant gastric cancers (75.0%) than in the primary gastric cancers (25.5%) (P < 0.0001). CONCLUSIONS: This information may help in the analysis of the carcinogenesis of gastric cancer; there is also a possibility that the COX-2 selective inhibitor to the remnant gastric cancer has a chemopreventive effect.     

Gastric adenocarcinoma and Helicobacter pylori infection.

Helicobacter pylori infection, thought to be causally related to chronic gastritis, may also be associated with an increased risk of gastric cancer. To determine whether an association with gastric cancer does exist, we retrospectively evaluated serum samples from 69 patients with histologically confirmed gastric adenocarcinoma (32 with cancer at the cardia and 37 with cancer at other sites) and from 218 patients with one of three categories of nongastric cancers, with other gastric cancers, or with benign gastric neoplasms. These samples were compared with samples from 252 cancer-free control subjects, a group comprising 76 asymptomatic volunteers and 176 persons with nonmalignant disorders. Serum samples collected from cancer patients prior to surgery and from cancer-free controls were tested for antibodies to H. pylori by using a highly sensitive and specific IgG enzyme-linked immunosorbent assay. The risk of H. pylori infection in the case patients relative to the control subjects was estimated with the use of multivariate logistic regression analysis to adjust for potential confounding variables. Antibodies to H. pylori were detected in 65% of the patients with noncardia gastric cancer but in only 38% of the patients with gastric cancer located at the cardia. A significant association was found between H. pylori infection and noncardia gastric cancer (odds ratio = 2.67; 99% confidence interval = 1.01-7.06). Within the subset of patients with noncardia gastric cancer, a statistically nonsignificant tendency existed for those with the intestinal versus the diffuse histologic type of noncardia gastric cancer to have a higher risk of H. pylori infection. Our results support the hypothesis of a relationship between H. pylori infection and the development of noncardia gastric adenocarcinoma.     

Association of Helicobacter pylori Infection with Gastric Adenocarcinoma

Gastric adenocarcinoma is the most prevalent cancer in South Korea, and Helicobacter pylori (H. pylori) infection is also common. This study was performed to examine the association between H. pylori infection and gastric cancer, taking into account various other factors. To investigate the association between gastric adenocarcinoma and H. pylori infection, determined by urease-positive reaction in the CLO test, a total of 175 paired specimens (175 tumor and 175 tissues adjacent to tumor) of stomach cancer patients and a total of 113 control specimens were obtained. The positive H. pylori infection rates were 78.9% (138/175) among the patients in specimens of tumor or tissues adjacent to the tumor and 41.6% (47/113) among controls in the CLO test. A positive correlation between H. pylori infection and gastric cancer was observed (age-adjusted odds ratio, 7.0; MH χ²=34.5 with P <0.0005). These data suggest that stomach cancer patients in Korea have high infection rates of H. pylori regardless of site specificity, and this infection might be causally associated with stomach cancer.     

Profiles of Epstein-Barr Virus Associated Gastric Carcinomas in Brunei Darussalam

Background: Gastric cancer is the second most common gastrointestinal cancer and is largely attributedto Helicobacter pylori (H. pylori) infection. In addition, studies have also shown association with Epstein-Barrvirus (EBV) in 10% of gastric cancers. This study assessed the characteristics of EBV associated gastric cancers(EBVaGC) in Brunei Darussalam. Materials and Methods: This study included gastric cancers diagnosed between2008 and 2012, registered with the Department of Pathology RIPAS Hospital, Brunei Darussalam. Clinical casenotes were systematically reviewed. Histology specimens were all stained for EBV and also assessed for intestinalmetaplasia and H. pylori. Results: There were a total of 81 patients (54 male and 27 females) with a mean age of65.8±14.8 years included in the study. Intestinal metaplasia and active H. pylori infection were detected in 40.7%and 30.9% respectively. A majority of the tumors were proximally located (55.6%), most poorly differentiated(well differentiated 16%, moderately differentiated 30.9% and poorly differentiated 53.1%) and the stages atdiagnosis were; stage I (44.4%), stage II (23.5%), stage III (8.6%) and stage IV (23.5%). EBV positivity (EBVaGC)was seen in 30.9%. Between EBVaGC and EBV negative gastric cancers, there were no significant differences(age, gender, ethnic group, presence of Intestinal metaplasia, tumor locations, stages of disease and degree oftumor differentiation). Conclusions: This study showed that a third of gastric cancers in Brunei Darussalamwere positive for EBV, higher than what have been reported in the literature. However, there were no significantdifferences between EBVaGC and EBV negative gastric cancers. This suggests that the role of EBV in gastriccancer may be mostly incidental rather than any causal relation. However, further studies are required.     

胃癌和癌前病变中幽门螺杆菌感染和增殖细胞核抗原,p53,c—erbB— …

目的 探讨幽门螺杆菌感染在胃癌发生发展中的作用。方法 对７０胃癌、６２例癌前病变和１６例对照组,应用改良Ｗａｒｔｈｉｎ－ｓｔａｒｒｙ法检测Ｈｐ,免疫酶组化ＳＰ法检测增殖细胞核抗原（ＰＣＮＡ）、ｐ５３、ｃ－ｅｒｂＢ－２等蛋白。结果 ＨＰ杂率在胃癌和癌前病变组均高于对照组,而前两组间差异无显著性,肠型和约漫型胃癌间ＨＰ感染率差异亦无显著性;胃癌和癌前病变组中,ＨＰ感染与ＰＣＮＡ表达、ｃ－ｅｒｂＢ－２过     

Sodium intake, salt taste and gastric cancer risk according to helicobacter pylori infection, smoking, histological type and tumor site in china

Aim: The risk factors mostly strongly associated with gastric cancer are gastric bacteria Helicobacter pyloriand diet. Using a case-control study among residents in Jinan, we examined the association between the salt tasteand gastric cancer according to H. pylori infection, smoking and histological type as well as tumor site. Methods:This population-based case-control study included 207 cases and 410 controls. Data on potential risk factors ofgastric cancer were obtained by interview of cases and controls with a questionnaire, salt taste preference wasmeasured for all subjects, and IgG antibodies to H. pylori were applied to assess infection. Risk measures weredetermined using unconditional logistic regression. Results: The proportions of salt taste at intervals of 1.8-7.2g/L and ≥7.2 g/L were significantly higher in cases than controls, with ORs of 1.56 (1.23-3.64) and 2.03 (2.12-4.11), respectively, subjects with high salt intake having an elevated risk for gastric cancer when infected withH. pylori. Significant modification by smoking and tumor site was observed across the different measures of saltintake, the highest salt taste showed higher cancer risk in ever smokers or with non-cardia cancers. Conclusion:Our study supports the view that high intake of sodium is an important dietary risk factor for gastric cancer,with a synergistic effect found between salt and H.pylori and smoking, dependent on the tumor site.     

Diffuse submucosal cysts of the stomach associated with gastric cancer: contribution of Helicobacter pylori infections

Diffuse submucosal cysts (DSCs) in the stomach are often associated with gastric cancer and a high occurrence of multiple gastric cancers. We studied the clinicopathological features of four early gastric cancer patients with DSCs in the submucosal layer of the stomach. All patients had early gastric cancers with gastritis and erosion in the gastric mucosa, and were positive for Helicobacter pylori (H. pylori). Based on a review of the reported cases, we found that a very high proportion (>94%) of DSCs are associated with infection by H. pylori. Although DSCs have previously been considered to be paracancerous lesions of gastric cancer, we speculate that DSCs might be post-inflammatory changes following infection by H. pylori, which may result in the high incidence of gastric cancer development.