吲哚胺2,3-双加氧酶1对幽门螺旋杆菌免疫调节的研究进展

幽门螺旋杆菌(Helicobacter pylori,H.pylori)是一种广泛黏附定植于胃黏膜的革兰阴性杆菌,流行病学研究显示,H.pylori感染是慢性胃炎的主要病因,长期停留于胃内可能导致慢性浅表性胃炎、慢性萎缩性胃炎、肠化生、异型增生和最终胃癌的发生;吲哚胺2,3-双加氧酶1(indoleamine 2,3-dioxygenase1,IDO1)是一种免疫调节酶,可在炎症过程中激活,诱导免疫耐受而有助于细菌长期生存;本文对胃黏膜中IDO1表达对H.pylori及H.pylori感染胃黏膜疾病发展的免疫调节作一概述。     

胃黏膜TGF-β1在幽门螺杆菌感染中的表达及与外周血T细胞亚群变化的关系

目的:探讨幽门螺杆菌(H.pylori)感染、TGF-β1及T淋巴细胞亚群在胃黏膜癌变过程中的作用及相互关系.方法:选取不同胃黏膜病变组织的72例胃镜活检标本,采用快速尿素酶试验(rapid urease test,RUT)结合Giemsa染色判断H.pylori感染,免疫组织化学染色技术检测胃黏膜组织中TGF-β1表达,流式细胞术检测不同胃黏膜病变患者外周血T淋巴细胞亚群CD3+、CD4+、CD8+及CD4+/CD8+比值.结果:TGF-β1在慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、肠上皮化生及不典型增生(IM/Dy)和胃癌(GC)中表达的阳性率分别为39.1%,52.6%,62.3%和87.5%,CSG组与IM/Dy、GC组相比,差异有统计学意义(P<0.05);IM/Dy中H.pylori阳性者TGF-β1表达明显高于H.pylori阴性者(87.5% vs 33.3%,P<0.05).与CSG相比,GC中CD3+明显降低(P<0.05),CD4+及CD4+/CD8+明显降低(P<0.01);IM/Dy患者CD4+及CD4+/CD8+低于CSG,有显著性差异(均P<0.01).不同胃黏膜病变TGF-β1表达与CD3+、CD4+T细胞、CD4+/CD8+呈负相关.结论:在GC前病变中,AKCSG到GC,TGF-β1表达逐渐增加,细胞免疫功能降低,TGF-β1对细胞免疫功能的抑制作用是IM/Dy、GC患者细胞免疫功能低下的原因之一.     

紧密连接蛋白Occludin及ZO-1在根除幽门螺杆菌慢性胃炎组织中的表达

目的观察闭锁蛋白(Occludin)及闭锁小带蛋白(zonula occludens-1,ZO-1)在根除幽门螺杆菌(Helicobacter pylori,H.pylori)慢性胃炎组织中的表达变化,探讨其与患者临床病理及预后的关系。方法采用免疫组织化学法检测H.pylori阴性正常人(25例)、根除H.pylori前后慢性浅表性胃炎(30例)及慢性萎缩性胃炎(30例)患者胃窦黏膜标本中Occludin、ZO-1的蛋白表达。结果 H.pylori阴性的正常人胃黏膜Occludin、ZO-1蛋白表达较H.pylori阳性慢性胃炎患者高,差异有统计学意义(P0.05),H.pylori阳性的慢性浅表性胃炎组织Occludin及ZO-1蛋白表达较慢性萎缩性胃炎增强,差异有统计学意义(P0.05);H.pylori根除治疗后,慢性浅表性胃炎组织中Occludin及ZO-1表达量较治疗前增强(P0.05),慢性萎缩性胃炎组织Occludin、ZO-1表达无明显变化(P0.05);H.pylori未根除患者,Occludin及ZO-1蛋白变化差异无显著性(P0.05)。结论 H.pylori阳性的慢性胃炎患者胃黏膜屏障受损,萎缩发生前根除H.pylori治疗可提高Occludin及ZO-1蛋白表达,进而修复H.pylori引起的胃黏膜损伤。     

袁红霞教授用经方辨治慢性萎缩性胃炎癌前病变经验撷菁

正胃癌前病变是一个病理性概念,是指较易转变为胃癌组织的病理学变化,包括肠上皮化生(IM)和异型增生(Dys),是正常胃黏膜向胃癌转化过程中的一个重要阶段~[1]。慢性浅表性胃炎→慢性萎缩性胃炎→肠上皮化生→异型增生→胃癌的Correa级     

胃癌高发区人群胃黏膜病变与细胞增殖、凋亡的关系

目的:研究山东省临朐县胃癌高发区人群中胃黏膜病变与细胞增殖、凋亡的关系.方法:通过对1523例受试者进行胃内窥镜检查,在胃内不同部位取胃黏膜活检进行病理学诊断,明确胃黏膜病变的分布.采用免疫组化方法检测Ki-67表达,采用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TINEL),评价不同病变细胞凋亡状况.结果:在受检人群中,93.8%患有慢性萎缩性胃炎、肠上皮化生或异型增生.各种病变在胃内分布不同,在胃体大弯处,正常或浅表性胃炎占84.56%,异型增生仅占0.07%,而在胃角处正常或浅表性胃炎为19.19%,而异型增生则为5.26%.研究还发现,细胞增殖与病变程度相对应,随着病变的加重,增殖趋于活跃,不同病变之间存在明显差异,但细胞凋亡程度未见明显差异(P=0.159).结论:在大样本人群研究中,明确了肠上皮化生、异型增生等癌前病变与胃癌发生部位的一致关系及细胞增殖和凋亡的失调.     

幽门螺杆菌感染对老年人胃黏膜环氧合酶-2表达的影响及意义

目的:评估幽门螺杆菌(H pylori)感染对老年人胃黏膜COX-2表达的影响及意义.方法:取不同阶段的胃黏膜病变共200例,用速尿素酶试验结合组织学Giemsa染色或14C尿素呼气试验检测胃黏膜H pylori感染状况,应用免疫组织化学检测胃黏膜上皮细胞COX-2的表达.结果:不同组织类型H pylori检出率以胃癌最高,其次为不典型增生(AH)和肠上皮化生(IM).COX-2在慢性浅表性胃炎(CSG)、IM、AH和胃癌中的表达阳性率分别为8%、24%、46%和64%,呈递增趋势,其阳性率胃癌与非癌组织相比差异均有统计学意义(P<0.01).同一类型 H pylori 阳性组COX-2的表达高于H pylori 阴性组,2组比较有显著性差异(P＜0.05).结论:COX-2表达上调与H pylori感染的胃黏膜的癌变有关,可能在癌前病变早期阶段起作用.     

慢性萎缩性胃炎与胃癌

萎缩性胃炎是指胃的固有腺体数目减少甚至消失,常伴有广泛的肠上皮化生和异型增生,肠上皮化生及异型增生为胃癌的癌前病变。正常胃黏膜．浅表性胃炎一萎缩性胃炎一肠上皮化生一异型增生一胃癌是Correa提出的慢性胃炎向胃癌演变的规律模式,已得到相关学者的广泛认同。越来越多证据表明,慢性萎缩性胃炎作为一种癌前疾病与胃癌的发生及发展密切相关。     

艾滋病患者消化系统表现、上消化道黏膜病变特点及相关因素

目的:研究艾滋病(acquired immune deficiency syndrome,AIDS)患者消化系统表现、上消化道黏膜病变特点及相关因素.方法:以有消化道症状且经胃镜检查有胃黏膜病变的127例AIDS患者为观察组,另选择同期收治的无消化道症状且经胃镜检查无消化道黏膜病变的120例AIDS患者为对照组.分别予以2组患者电子胃镜检查及幽门螺杆菌(Helicobacter pylori,H.pylori)检测,并取2组患者胃黏膜组织行CD-38及Ki-67免疫组织化学检测.结果:观察组127例AIDS患者消化系统症状由主到次表现为腹胀、腹痛、腹泻等;观察组AIDS患者上消化道黏膜病变特点表现为慢性浅表性胃炎、慢性萎缩性胃炎、念珠菌性食管炎等,且其中慢性浅表性胃炎(40.94%)与慢性萎缩性胃炎(20.47%)的比例显著高于其他黏膜病变(P0.05).对照组患者H.pylori感染率为10.83%,观察组为12.60%,2组比较,差异无统计学意义(P0.05).观察组患者胃黏膜组织CD-38阳性表达高于对照组(P0.05),Ki-67阳性表达低于对照组(P0.05).结论:AIDS患者消化系统表现以腹胀、腹痛、腹泻为主,上消化道黏膜病变以慢性浅表性胃炎、慢性萎缩性胃炎为主,胃黏膜组织CD-38高表达及Ki-67低表达可能是诱发AIDS患者出现消化系统症状的重要因素.     

尿素循环限速酶CPS1在胃黏膜肠上皮化生及癌变过程中的表达特征

目的探讨尿素循环限速酶氨甲酰磷酸合成酶1(CPS1)在胃黏膜肠上皮化生及癌变过程中的表达特征。方法采用免疫组织化学法检测10例胃浅表黏膜慢性炎、10例小肠黏膜慢性炎、10例结肠黏膜慢性炎、32例慢性萎缩性胃炎伴肠化生、30例低度异型增生、32例高度异型增生中CPS1、CDX2的表达及172例肠型胃癌组织芯片中CPS1的表达。结果 CPS1和CDX2在胃黏膜中均无阳性表达。CDX2在小肠、结肠黏膜中均呈阳性表达,而CPS1仅在小肠黏膜中表达。CPS1强阳性表达率在肠化生占100%(32/32),低度异型增生占70.0%(21/30),高度异型增生占12.5%(4/32),肠型胃癌占8.1%(14/172)。CPS1的表达率在癌变各个阶段间差异有统计学意义(P0.05)。CDX2在肠化生、低度异型增生、高度异型增生中强阳性表达率为87.5%(28/32)、100%(30/30)和78.1%(25/32)。CDX2在低度异型增生、高度异型增生间差异有统计学意义(P=0.0118)。在胃腺癌中,CPS1表达下调与浸润深度和TNM分期显著相关。结论本研究支持CPS1和CDX2均是鉴别胃黏膜肠上皮化生病变的特异性标志物;与CDX2相比,CPS1在高度异型增生及腺癌阶段表达下调,提示CPS1表达下调可能是肠化生恶性转变的标志物;CPS1表达下调与临床分期呈正相关,提示CPS1可能是肠型胃癌的抑癌基因。     

慢性萎缩性胃炎伴异型增生的治疗进展

慢性萎缩性胃炎伴胃黏膜异型增生属于癌前病变。目前国内外学者一致认同肠型胃癌发生的Correa模式[1]即＂正常胃黏膜—慢性浅表性胃炎—慢性萎缩性胃炎—肠上皮化生—异型增生—胃癌＂的发展模式。如能对胃黏膜异型增生进行积极的随访监测,并加以有效干预,从而阻断其向胃癌发展,那将显著降低胃癌的发生率和病死率。     

幽门螺杆菌感染者胃粘膜癌前病变与Fas抗原表达的关系

目的研究幽门螺杆菌(Hp)感染后胃粘膜癌前病变中 Fas 抗原表达的情况,了解 Hp 在胃癌发生过程中的作用。方法采用免疫组织化学等方法检测83例经病理证实为慢性胃炎病人胃粘膜上皮细胞中 Fas 抗原的表达情况。结果在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,Fas 抗原表达率分别为20.00%、36.36%、73.33%、43.75%,Fas 抗原在肠化生中的表达率显著高于浅表性胃炎、萎缩性胃炎及异型增生(P<0.01及P<0.05)。Hp 感染者 Fas 抗原表达率为60.71%,显著高于 Hp 阴性者的22.22%(P<0.01)。在萎缩、肠化生及异型增生等癌前病变中,Hp 感染者与未感染者表达率分别为65.96%及28.57%(P<0.01)。结论 Hp 感染对 Fas 抗原表达有一定的影响,Hp 感染可促进 Fas 抗原表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。     

Expression of gastric cancer—associated MG7 antigen in gastric cancer,precancerous lesions and H.pylori—associated gastric diseases

AIM: To investigate the relationship between the antigen MG7 antigen expression and gastric cancer as well as precancerous condition; to study the relationship between the MG7 antigen expression and H. pyloriinfection in benign gastric lesions in order to find out the effect of H. pylori infection on the process of gastric cancer development.METHODS: The level of MG7 antigen expression was determined by immunohistochemical method in 383 gastric biopsied materials. The intestinal metaplasia was determined by histochemistry method. The H. pyloriinfection was determined by HE stain, PCR and ELISA in 291 specimens, among which only 34 cases of H. pylori-associated gastric lesions were followed up.RESULTS: The positive rate of MG7 expression in normal gastric mucosa, intestinal metaplasia, dysplasia and gastric cancer increased gradually in ascending order (P＜0.01). The positive rate of MG7 antigen expression in type Ⅲ intestinal metaplasia of gastric mucosa was higher than that of type Ⅰand Ⅱ intestinal metaplasia, being highly significant (P＜0.05).The positive rate of MG7 antigen expression in superficial gastritis, atrophic gastritis and gastric cancer increased gradually (11.9 %, 64.8 %, 91.2 %, P＜0.01). There was no significant difference between H.pylori-negative and H. pyloripositive intestinal metaplasia, atrophic gastritis and dysplasia of gastric epithelium in the positive rate of MG7 antigen expression. There was no expression of MG7 antigen in H. pylori-negative superficial gastritis. The positive rate of MG7 expression in H. pylori-positive superficial gastritis was 20.5 %, and the difference between them was significant (P＜0.05). During following up, one of the three H. pylori negative cases turned positive again, and its MG7 antigen expression turned to be stronger correspondingly. 3 of 31 H. pyloripositive cases were detected as early gastric cancer, among which one with "+++" MG7 antigen expression was diminished after H. pylori eradication.CONCLUSION: MG7 antigen expression is highly specific in gastric cancer and can be used as a good marker for screening of gastric cancer; type Ⅲ intestinal metaplasia, atrophic gastritis and dysplasia should be followed up and MG7 antigen expression has high clinical value in the dynamic follow-up study; although the positive -MG7 in positiveH. pylorisuperficial gastritis show benign morphology in features, there is still the potential risk of developing into gastric cancer, hence special attention should be paid to those showing increasing MG7 antigen expression.     

胃粘膜癌前病变中幽门螺杆菌与c-met原癌基因蛋白表达关系的研究

为研究Hp感染后胃粘膜细胞中c-met原癌基因蛋白表达的情况,了解Hp在胃癌发生过程中的作用,对110例经病理证实为慢性胃炎的病人用免疫组化方法检测了胃粘膜细胞中e-met原癌基因蛋白表达情况。结果表明,在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,e-met原癌基因蛋白的表达率分别为22.2％、44.1％、67.5％和61.9％。过表达率分别为5.5％、26.4％、37.8％和38.1％。Hp感染后c-met原癌基因蛋白表达率较末感染者高,分别为63％及32％,在萎缩,肠化生及异型增生等癌前病变中Hp感染者与未感染者表达率分别为58.9％及29.7％(P<0.005)。本研究结果显示,随着病变的进展,c-met原癌基因的表达随之增加,从而说明Hp感染对c-met原癌基因蛋白表达有一定的影响,Hp启动了胃癌发展的早期阶段,也可能推进胃癌的发展过程。     

Prevalence of Helicobacter pylori infection and gastric cancer precursor lesions in patients with dyspepsia

BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.     

胃癌及癌前病变中P57~(KIP2)和PCNA的表达

探讨P57KIP2和PCNA在胃癌及癌前病变中的表达及意义。方法采用免疫组织化学技术SP法,检测P57KIP2和PCNA在57例胃癌(GC)、7例不典型性增生(Dys)、16例肠上皮化生(IM)、15例慢性萎缩性胃炎(CAG)及10例慢性浅表性胃炎(CSG)中的表达情况,并分析与胃癌临床病理之间的关系。结果P57KIP2在GC、Dys、IM、CAG、CSG中阳性表达率分别为43.9%、57.1%、81.3%、80.0%、80.0%,GC和Dys组的P57KIP2阳性表达率明显低于IM、CAG、CSG组(P均0.05);PCNA在GC、Dys、IM、CAG、CSG组阳性表达率分别为80.7%、85.7%、75.0%、46.7%、30.0%,GC、Dys、IM组PCNA表达率明显高于CAG、CSG组(P0.05);P57KIP2和PCNA均与胃癌组织分化程度相关(P0.05),而与淋巴结转移、浸润、临床分期无显著相关性(P0.05)。结论在胃黏膜癌变过程中,P57KIP2蛋白的失活不是一个早期基因事件,随着病变进展PCNA表达逐渐增加,P57KIP2蛋白表达下降和PCNA的表达增高可能在胃癌的发生发展中起重要作用,两者共同检测有助于胃癌恶性程度的判定。     

原位杂交方法检测胃癌及其癌前病变中抑癌基因p53的表达

目的用原位杂交方法检测胃粘膜癌前病变及胃癌组织中ｐ５３ｍＲＮＡ的表达,并观察感染Ｈｐ对其表达的影响．方法病理证实为慢性胃炎６６例和胃癌１６例,用地高辛标记的ｃＤＮＡ为探针进行原位杂交实验,检测其胃粘膜组织中ｐ５３ｍＲＮＡ表达,用单克隆抗体ＤＯ０１进行免疫组化检测Ｐ５３蛋白的表达．结果在慢性萎缩性胃炎、肠化生、异型增生及胃癌中,原位杂交方法检测ｐ５３ｍＲＮＡ表达率分别为５３９％,５２３％,４２８％和２５％,免疫组化方法检测Ｐ５３蛋白的表达率分别为００％,５３％,１５４％和２５％．ｐ５３ｍＲＮＡ的表达与蛋白的表达无明显的一致性,ｐ５３ｍＲＮＡ的表达可以在Ｐ５３蛋白阴性及阳性的细胞中．在２６例萎缩性胃炎中,１４例检测到ｐ５３ｍＲＮＡ的表达,而其中１６例（包括１４例阳性病例）无一例检测到Ｐ５３蛋白的表达．在肠化生、异型增生及胃癌组织中也发现有类似的情况．Ｈｐ感染组与未感染组,ｐ５３ｍＲＮＡ表达率之间统计学检验Ｐ＜００５．结论在胃癌及其癌前病变中,随着病变的发展,ｐ５３ｍＲＮＡ的表达率随之下降,Ｈｐ对其表达有明显的影响     

Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases

AIM: To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori (H pylori) as a risk factor for gastric cancer. METHODS: One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay (PCR-ELISA), and c-Myc expression using immunohistochemistry. RESULTS: The telomerase activity and c-Myc expression were higher in cancers (87.69% and 61.54%) than in noncancerous tissues. They were higher in chronic atrophic gastritis with severe intestinal metaplasia (52.38% and 47.62%) than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%). In chronic atrophic gastritis with severe intestinal metaplasia, the telomerase activity and c-Myc expression were higher in cases with H pylori infection (67.86% and 67.86%) than in those without infection (21.43% and 7.14%). c-Myc expression was higher in gastric cancer with H pylori infection (77.27%) than in that without infection (28.57%). The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION: H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.     

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.     

胃癌前组织和胃癌中hTERT、Bcl-2蛋白的表达及其相互关系

目的 探讨胃癌前组织及胃癌中人端粒酶催化亚单位(human telomerase catalytic subunit,hTERT)的表达状况及其与Bcl-2蛋白表达的关系。方法 应用免疫组织化学技术检测45例慢性胃炎和19例胃癌中hTERT和Bcl-2蛋白的表达。结果 hTERT蛋白表达率在萎缩性胃炎、肠化生、异形增生和胃癌等不同胃黏膜癌变过程中呈递增趋势;hTERT蛋白的表达率在胃癌组织中显著高于异形增生、肠化生和萎缩性胃炎组织(P<0.05);在异形增生组织中显著高于肠化生和萎缩性胃炎组织(P<0.05);在肠化生组织中显著高于萎缩性胃炎组织(P<0.05)。Bcl-2蛋白表达率在萎缩性胃炎、肠化生、异形增生和胃癌等不同胃黏膜癌变过程中呈递增趋势;Bcl-2蛋白的表达率在胃癌组织中显著高于异形增生、肠化生和萎缩性胃炎组织(P<0.05);在异形增生组织中显著高于萎缩性胃炎组织(P<0.05),亦高于肠化生,但是相差无显著性;在肠化生组织中显著高于萎缩性胃炎组织(P<0.05)。Bel-2蛋白阳性患者hTERT蛋白表达率为71.43％,Bcl-2蛋白阴性患者hTERT蛋白表达率34.44％,hTERT蛋白表达率在Bcl-2蛋白阳性患者中显著高于Bcl-2蛋白阴性患者(P<0.01)。结论 在胃癌和胃癌前病变阶段,端粒酶(telomerase)与Bcl-2均可能发挥重要作用,促进了胃癌的发生、发展;Bcl-2表达增加可能是胃     

胃黏膜癌前病变中p53、p21^ras蛋白表达与幽门螺杆菌感染的关系

目的观察幽门螺杆菌(Helicobacterpylori)感染及根除H.pylori二年后p53、p21ras在二组胃黏膜上皮细胞的表达,探讨H.pylori在胃癌发生、发展中的作用.方法应用免疫组织化学染色、尿素酶快速试验(RUT)、组织学Warthin-Starry染色.198例H.pylori感染患者,慢性胃炎86例,慢性胃炎伴肠化生67例,慢性胃炎伴异型增生45例;对照组为根除H.pylori 2年后共86例,其中慢性胃炎54例,慢性胃炎伴肠化生32例,慢性胃炎伴异型增生10例.全部病例做p53、p21ras免疫组织化学染色.结果 H.pylori感染组p53、p21 ras 阳性表达率15.7%、18.7%,明显高于H.pylori根除组2.3%、7%,差异显著(P＜0.05);慢性胃炎伴肠化病变中,p53、p21ras在H.pylori感染组阳性表达率17.9%、18.4%均高于H.pylori根除组0%、9.4%,差异显著(P＜0.05)慢性胃炎伴异型增生病变中,p53、p21 ras在H.pylori感染组阳性表达率31.1%、40%均高于H.pylori根除组20%、30.4%,差异显著(P＜0.05);H.pylori 感染组p53、p21ras在慢性胃炎,肠化生,异型增生表达水平依次增高p53、p21ras共同表达阳性37例.结论在胃黏膜癌前病变中p53、p21ras 在H.pylori感染组阳性表达率高于H.pylori根除组,差异显著(P＜0.05);在慢性胃炎,肠化生,异型增生p53、p21ras表达水平在增高;p53、p21 ras表达呈正相关;H.pylori感染在胃癌发生、发展过程中起一定作用,p53、p21ras表达可能是H.pylori致癌的作用机理之一.