幽门螺杆菌感染患者胃癌及癌旁组织中p53、p16和bcl-2基因的表达

目的:研究幽门螺杆菌(H.pylori)感染胃癌患者胃粘膜病变中抑癌基因p53、p16和关键性凋亡调节基因bcl-2蛋白的表达,进一步探讨H.pylori在胃癌发生、发展过程中作用的分子机制.方法:胃镜检查及外科手术中取40例胃癌患者的癌组织和癌旁2 cm处组织各2块,石蜡包埋,切片HE染色作病理诊断及免疫组化检测p53、p16及bcl-2蛋白的表达.H.pylori阳性由快速尿素酶试验结合病理染色/14C-尿素呼气试验确定.结果:40例胃癌患者中,H.pylori阳性23例,阴性17例.p53阳性表达率在H.pylori阳性及阴性胃癌组织中无显著差异(P＞0.05).H.pylori阳性组慢性胃炎或肠化组织中p16的阳性表达率及表达强度均显著低于H.pylori阴性组(表达率:P＜0.05;表达强度:P＜0.001和P＜0.01).而H.pylori阳性组肠化组织中bcl-2的阳性表达率及表达强度均显著高于H.pylori阴性组(P＜0.05).结论:在胃癌发生的早期即存在较明显的p16基因表达低下与bcl-2基因过度表达,并与H.pylori感染有一定关系.p53基因过度表达是胃癌发展过程中较晚期的事件,与H.pylori感染无明显相关性.     

胃癌组织中livin与caspase-9、p53的表达及相互关系

目的 研究凋亡蛋白livin和 caspase-9、p53在胃癌组织中的表达及与胃癌生物学行为关系.方法采用免疫组化S-P检测58例胃癌组织及正常胃黏膜中livin和caspase-9、p53的蛋白表达.结果胃癌组织中 livin和caspase-9的、p53蛋白表达阳性率分别为65.5%、20.7%、58.6%,与正常胃黏膜蛋白表达阳性率(分别为3.5%、62.1%、5.2%)比较差异有统计学意义(P＜0.05);livin在组织分化差、淋巴结转移者、临床分期高表达率均增高差异有显著性(P＜0.05);livin表达与caspase-9蛋白表达呈负相关性(rs=-0.195,P＜0.05).livin与p53蛋白表达呈正相关性(rs= 0.851,P＜0.05).结论 livin和caspase-9参与胃癌的发生、发展,可能成为胃癌治疗的新分子靶点.抑癌基因p53的失活与凋亡抑制基因livin在胃癌的发生方面可能有相互促进作用.     

胃粘膜肠化及异型增生和胃癌组织中多基因异常

目的 探讨多种基因改变在癌前病变及胃癌组织中的作用.方法 应用PCR-RFLP,PCR-SSCP,RT-PCR及免疫组化技术同时对60例肠化生,30例异型增生及52例胃癌组织中抑癌基因APC,MCC,DCC,YNZ22,p53及癌基因Ki-tas,Bcl-2多种变异形式进行检测.结果 随着肠化生粘膜向异型增生、胃癌的发展,多种基因改变的频率逐步升高,胃癌组织中APC,DCC,YNZ22,p53,Bcl-2的改变频率分别为57.7%(30/52),43.1%(22/51),51.6%(16/31),67.3%(35/52),68.6%(35/51)显著高于肠化生上述基因的改变(APC 33.3%,DCC 4.3%,YNZ22 19.4%,p5326.7%,/Bcl-2 33.3%)(P＜0.05,0.01).异型增生组织中DCC基因改变为12.5%(3/24),也显著低于胃癌组织中的改变.Ⅲ型肠化中APC及bcl-2基因蛋白表达率分别为61.1%,55.6%,p53突变及蛋白表达率为57.1%,27.8%,显著高于I,Ⅱ型肠化中APC,Bcl-2蛋白表达率(6.3%,23.8%)(P＜0.01,0.05)及p53突变及蛋白表达率(18.2%,2.4%)(P＜0.05).肠型胃癌APC,p53,Ki-ras突变率分别为52.9%;82.4%;29.4%,显著高于胃型胃癌各基因的突变(APC 18.2%;p53 45.8%;Ki-raS 3.0%)(P＜0.05).肠型胃癌APC,Ki-ras,bcl-2基因的蛋白表达率分别为76.5%;41.2%;93.8%,胃型胃癌分别为30.3%;3.0%;54.5%,两型相比差别显著(P＜0.01,0.05).APC,p53及Bcl-2基因可能是肠化生癌变及肠型胃癌的热点基因.肠化生及异型增生阶段即可检测到基因改变的累积现象,但以胃癌组织中最显著.结论 多种基因改变的累积与胃癌的发生及演进密切相关.不同类型肠化生分子改变机制不同.APC,p53及Bcl-2基因有可能成为肠型胃癌早期诊断的分子标志.     

幽门螺杆菌感染胃癌癌旁组织p53、p16和bcl-2基因的表达

目的:研究幽门螺杆菌(H·pylori)感染胃粘膜病变抑癌基因(p53、p16)和关键性凋亡调节基因bcl-2蛋白的表达,进一步探讨H·pylori在胃癌发生发展过程中作用的分子机制。方法:胃镜、外科手术中取40例胃癌患者的癌组织、癌旁组织(靠近癌的正常组织)各两块,石蜡包埋。切片HE染色作病理及免疫组织化学检查p53、p16、bcl-2蛋白表达。H·pylori阳性由CLOtest结合病理染色/~(14)C尿素呼吸试验而确定。结果:p53阳性表达率在H·pylori阳性及阴性胃癌组之间无显著性差别(p>0.05)。H·pylori阳性组慢性胃炎或肠化中p16阳性表达率及阳性表达强度均显著低于H·pylori阴性组(p<0.05,p<0.01)。而H·pylori阳性组肠化中bcl-2阳性表达率及阳性表达强度均显著高于H·pylori阴性组(pall<0.05)。结论:在胃癌发生的早期即存在较明显的p16基因表达低下与bcl-2基因过度表达,并与H·pylori感染有一定的关系。p53基因过度表达是胃癌发展过程中较晚期事件,与H·pylori感染无明显相关性。     

肠化生、胃癌组织中幽门螺杆菌感染与ras基因表达

螺杆菌(Hp)感染引起慢性活动性胃炎、萎缩性胃炎、肠腺化生、不典型增生,最终导致肠型胃癌的链状改变虽被公认,但并非Hp高感染率的地区胃癌的发生率一定升高.胃癌的发生、发展是癌基因的突变与抑癌基因失活逐渐演变的复过程,而癌基因突变与抑癌基因失活并非Hp单一因素,而是多因素参与的结果.通过病理染色、快速尿素酶试验检测Hp感染,免疫组织化学染色检测P21蛋白,了解在肠化生、胃癌组织中Hp感染与ras基因表达之间的关系.     

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.     

P53Arg72Pro多态性及H pylori感染与胃癌高发区甘肃河西地区胃癌的关系

目的:检测H pylori在甘肃河西地区健康人群与胃癌患者中的感染,并探讨P53Arg72Pro基因多态性以及H pylori感染与胃癌高发区甘肃河西地区胃癌发生的关系.方法:采用PCR-TaqMan探针法检测甘肃河西地区健康人群和胃癌患者P53Arg72Pro的基因多态性,用Warhin-starry染色法检测本研究对象的H pylori感染率.结果:H pylori感染率在胃癌组和对照组分别为68.6%,50.4%,H pylori感染率在两组间具有显著差异(OR=2.147,95%CI:1.302-3.541);P53Arg72Pro分为Arg/Arg,Arg/Pro,Pro/Pro3 种基因型,其频率在胃癌患者中分别为15.7%,60.0%,24.3%;在健康人群中分别为25.6%,54.4%,20.0%.与Arg/Arg基因型相比,Arg/Pro或Pro/Pro单独频率在2组间差异无统计学意义,但P53Pro等位基因(Arg/Pro+Pro/Pro)携带者在胃癌者和对照组间差异有统计学意义(OR=1.846;95%CI:1.006-3.387).分层分析提示H pylori阳性感染者或吸烟人群,若其同时携带有P53Pro等位基因,他们患胃癌的风险明显增加.结论:P53Arg72Pro位点基因多态性与我国胃癌高发区甘肃河西地区胃癌发病的风险相关,P53Pro等位基因与H pylori感染或吸烟因素有一定的协同作用.     

幽门螺杆菌感染与TNM胃癌分期相关性的研究

目的探讨胃癌患者幽门螺杆菌(H.pylori)感染与不同TNM胃癌分期的相关性。方法通过~(14)C-UBT检测不同TNM分期胃癌患者H.pylori感染状况,对比不同TNM分期胃癌患者骨桥蛋白(OPN)及P53的表达与H.pylori感染的相关性。结果Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期胃癌患者H.pylori感染率分别为52.0%,68.0%、76.7%及84.0%;随着胃癌患者病情的发展H.pylori的感染率显著升高(P0.05)。Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期H.pylori阳性胃癌患者的P53表达率均显著高于H.pylori阴性患者(P0.05),且Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期胃癌患者H.pylori阳性与P53表达率呈正相关,Ⅳ期胃癌患者H.pylori阳性与P53表达率相关系数为0.752。Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期H.pylori阳性胃癌患者的OPN表达率均显著高于H.pylori阴性患者(P0.05),Ⅱ期、Ⅲ期、Ⅳ期胃癌患者H.pylori阳性与OPN表达率呈正相关,并随着胃癌病情加重相关性更为明显。结论胃癌Ⅲ期、Ⅳ期患者H.pylori感染率显著升高,且H.pylori感染与OPN表达率和P53表达率呈正相关,并随着胃癌病情的加深相关越紧密。     

幽门螺杆菌感染与胃癌及癌前病变中癌基因蛋白表达的关系

近年来,众多流行病学资料提示,幽门螺杆菌(Helicobacter pylori,Hp)感染与胃癌的Hp发生密切相关[1-4].动物实验证实,Hp慢性感染易引起胃粘膜组织恶性转化[2].但其致癌机制未明,更缺乏直接的分子生物学证据[5].作者通过研究Hp感染对胃粘膜细胞增殖动力学的影响以及与胃癌和胃粘膜炎性病变中癌基因蛋白P21,c-myc,c-erbB-2及抑癌基因蛋白P53表达的相关性,以进一步探讨Hp感染与胃癌发生的关系及其可能的致癌机制.     

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.     

Effect of Helicobacter pylori infection on Bax protein expression in patients with gastric precancerous lesions

AIM: To investigate the effect of Helicobacter pylori (H pylori) infection on Bax protein expression, and explore the role of H pylori in gastric carcinogenesis. METHODS: H pylori was assessed by rapid urease test and Warthin-Starry method, and expression of Bax protein was examined immunohistochemically in 72 patients with pre-malignant lesions. RESULTS: Bax protein was differently expressed in intestinal metaplasia and gastric dysplasia, and showed 63.99% positivity. The positivity of Bax protein expression in Hpylori-positive gastric precancerous lesions (72.3%) was significantly higher than that in H pylori-negative gastric precancerous lesions (48.0%, X~2=4.191, P<0.05). H pylori infection was well correlated with the expression of Bax protein in gastric precancerous lesions (r=0.978, P<0.01). After eradication of H pylori, the positivity of Bax protein expression significantly decreased in H pylort-positive gastric precancerous lesions (X~2=5.506, P<0.05). In the persisting H pylori-infected patients, the positivity of Bax protein expression was not changed. CONCLUSION: H pylori infection may be involved in the upregulation of Bax gene, which might be one of the mechanisms of H pylori infection-induced gastric epithelial cell apoptosis. H pylori might act as a tumor promoter in the genesis of gastric carcinoma and eradication of H pylori could inhibit gastric carcinogenesis.     

Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection, histological types and staging

AIM:To investigate the expression of multiple genes and the behavior of cellular biology in gastric cancer (GC) and other gastric mucosal lesions and their relations to Helicobacter pylori (H. pylori) infection, tumor staging and histological subtypes.METHODS:Three hundred and twenty seven specimens of gastric mucosa obtained via endoscopy or surgical resection, and ABC immunohistochemical staining were used to detect the expression of p53, p16, Bcl-2 and COX-2 proteins.H. pylori was determined by rapid urea test combined with patholo-gical staining or 14 Curea breath test. Cellular image analysis was performed in 66 patients with intestinal metaplasia (IM) and/or dysplasia (Dys). In 30 of them, both cancer and the paracancerous tissues were obtained at the time of surgery. Histolo-gical pattern, tumor staging, lymph node metastasis, grading of differentiation and other clinical data were studied in the medical records.RESULTS:p16 expression of IM or Dys was significantly lower in positive H. pylori chronic atrophic gastritis (CAG) than those with negative H. pylori (CAG: 54.8% vs 88.0%, IM:34.4% vs 69.6%, Dys: 23.8% vs 53.6%, all P < 0.05), Bcl-2 or COX-2 expression of IM or Dys in positive H. pylori cases was signi-ficantly higher than that without H. pylori (Bcl-2: 68.8% vs 23.9%, 90.5% vs 60.7%; COX-2: 50.0% vs 10.8%, 61.8% vs 17.8%; all P <0.05). The mean number of most parame-ters of cellular image analysis in positive H. pylori group was significantly higher than that in negative H. pylori group (Ellipser: 53 plus minus 14, 40 plus minus 12&mgr;m, Area(1): 748 plus minus 572, 302 plus minus 202&mgr;m(2), Area(2): 3050 plus minus 1661, 1681 plus minus 1990&mgr;m(2), all P< 0.05; Ellipseb: 79 plus minus 23, 58 plus minus 15&mgr;m, Ratio-1: 22% plus minus5%,13% plus minus4%,Ratio-2:79% plus minus17%,53% plus minus20%,all P<0.01). There was significant correl-ation between Bcl-2 and histologic pattern of gastric carcinoma, and between COX-2 and tumor staging or lymph node metasta sis (Bcl-2: 75.0% vs16.7%; COX-2: 76.0% vs 20.0%, 79.2% vs 16.7%; all P< 0.05).CONCLUSION:p16, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infec-tion. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.     

Association of H. pylori infection with gastric carcinoma: a Meta analysis

AIM:To follow the principles of evidence based medicine toreach the integrated results of these studies.METHODS:Twenty-one papers of caes-control studies wereselected,including 11 on gastric cancer,7 on precancerouslesion of stomach and 3 on lymphoma of stomach.Metaanalysis was used to sum up the odds ratios(OR)of thesestudies.RESULTS:H.pylorl vsgastric cancer(intestinal and diffusetype):the odds ratio from the fixed effect model is 3.0016(95% Cl:2.4197-3.7234,P<0.001).H.pylori vsprecancerous lesion of stomach:a random effect model wasused to calculate the summary odds ratio and its value is2.5635(95% Cl:1.8477-3.5566,P<0.01).H.pylori vslymphoma of stomach:though the quantity of literature istoo small to make Meta analysis,the data of these 3 studiesshow that lymphoma of stomach is highly associated withH.pylori infections.CoNCLUSION:Since it had been revealed that H.pyloriinfection pre-existo in gastric carcinoma and precancerouslesions,the results of Meta analysis present a strongevldenca to support the conclusion that H.pyiori infectionis a risk factor for gastric carcinoma.     

幽门螺杆菌感染和端粒酶活性以及c-myc、p16基因的表达在胃黏膜癌变中的相关性研究

幽门螺杆菌(H.pylori)是胃癌的主要致病因子,H.pylori、端粒酶和肿瘤相关基因的关系在胃黏膜癌变发生过程中研究很少。目的:观察H.pylori感染和端粒酶活性以及c-myc、p16基因在胃癌中的关系。方法:通过胃镜活检和外科手术获取171例胃组织标本,快速尿素酶试验和H.pylori培养确定有无H.pylori感染;酶联免疫法检测H.pylori感染患者的血清CagA-IgG水平;聚合酶链反应.酶联免疫吸附测定(PCR-ELISA)法检测端粒酶活性;免疫组化法检测c-myc、p16基因的表达。结果:胃癌(GC)组端粒酶表达率显著高于其他各组(P<0.01);慢性萎缩性胃炎(CAG)伴中、重度肠化(IM)组端粒酶和c-myc表达率显著高于CAG伴轻度IM组(P<0.05);而慢性浅表性胃炎(CSG)和CAG伴轻度IM组p16表达率显著高于CAG伴中、重度IM、异型增生(Dys)和GC组(P<0.05)。在CAG伴轻、中、重度IM组中,H.pylori阳性组端粒酶活性比阴性组高:无论有无H.pylori感染,胃癌组端粒酶活性都非常高。在CAG伴中、重度IM、Dys和GC组中,H.pylori阳性亚组c-myc表达显著高于阴性亚组(P<0.01),而在ECAG伴中、重度IM和Dys组中,H.pylori阳性亚组p16基因表达显著低于阴性亚组(P<0.01)。结论:H pylori感染很可能主要通过c-myc基因的激活和p16基因的失活以及其他基因的变化来诱导CAG伴中、重度     

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.     

胃癌中幽门螺杆菌感染与原癌基因c—met表达及预后研究

目的　研究幽门螺杆菌(Hp)感染的胃癌(GC)组织中c-met表达及(Hp)感染对胃癌预后的影响。方法　经病理证实,不同病变胃粘膜145例以免疫组化检测c-met基因表达,以W-S法及快速尿素酶试验检测(Hp)感染。结果　在浅表性胃炎(CSG)、萎缩肠化生胃炎(CAG+IM)、异型增生(DYS)、早期GC和进展期GC中,c-met基因表达率分别为25.53%,51.28%,61.54%,66.67%和68.42%,CAG+IM、DYS、GC均显著高于CSG(P＜0.05)。肠型胃癌c-met阳性表达与(Hp)感染密切相关。CAG+IM,DYS和GC组c-met阳性表达(Hp)感染者明显高于阴性组。(Hp)阳性者5年生存期显著短于(Hp)阴性者。结论　(Hp)感染和c-met表达与胃粘膜增殖和恶化有关,前者也与胃癌预后有关。     

幽门螺杆菌感染胃黏膜病变基因表达和细胞生物学行为

目的　研究幽门螺杆菌(Helicobacterpylori,Hp)感染胃黏膜病变的多基因表达和细胞生物学行为。方法　327例患者经胃镜及手术的胃黏膜病变标本,应用免疫组化染色法,检测p53、p16、bcl-2和环氧合酶同工酶-2(COX-2)蛋白的表达。Hp感染由快速尿素酶试验结合组织学检查/     

胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin6的表达及其与幽门螺杆菌感染的关系

目的探讨胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin 6(Prx6)表达水平变化及其与幽门螺杆菌(H.pylori)感染的关系。方法根据组织形态学将104例临床内镜检查活检标本分为慢性浅表性胃炎(33例)、慢性萎缩性胃炎(25例)、肠上皮化生(32例)及异型增生(14例)4组。用免疫组织化学方法检测组织标本中Prx6的表达水平。用快速尿素酶试验及Warthin-Starry银染检测H.pylori感染。结果 Prx6在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生组的阳性表达率分别为39.4%(13/33)、80.0%(20/25)、93.8%(30/32)、92.9%(13/14),过表达率分别为15.2%(5/33)、44.0%(11/25)、81.3%(26/32)、85.7%(12/14)。慢性浅表性胃炎、慢性萎缩性胃炎组H.pylori阳性者Prx6阳性表达率显著高于H.pylori阴性者(P<0.05),肠上皮化生组Prx6的表达在H.pylori阳性者和阴性者无显著差异(P>0.05)。结论在胃黏膜病变演化过程中,Prx6的表达随着胃黏膜病变的进展而增加,H.pylori在胃黏膜病变演化的早期阶段促进了Prx6的表达。     

Hp感染与胃癌和癌前病变中p53、ras、c-myc基因表达的关系

目的研究幽门螺杆菌（Hp）感染与胃癌（GC）和癌前病变中p53、ras、c-myc基因表达的关系,以探讨其致病机制。方法用美兰和W-S特殊染色方法确定Hp感染,免疫组化SP法检测p53、ras、c-myc基因的表达。结果慢性萎缩性胃炎（CAG）、肠化生（IM）、异型增生（DYS）、GC的Hp感染率均高于慢性浅表性胃炎（CSG）（P均〈0.05）;p53、ras、c-myc基因在GC、DYS中的表达均高于CAG（P均〈0.05）,p53、ras基因在IM中的表达均高于CAG（P〈0.05）;IM中Hp阳性者的p53阳性表达率高于Hp阴性者（P〈0.05）,DYS、GC中Hp阳性者p53、ras、c-myc的表达率高于Hp阴性者（P均〈0.05）。结论Hp感染可能通过调节p53、ras、c-myc基因的表达而促进GC的发生。