幽门螺杆菌与胃黏膜bFGF,FGFR-2表达的关系及意义

目的:探讨幽门螺杆菌(H pylori)感染的胃黏膜上皮细胞碱性成纤维细胞生长因子(bFGF)、成纤维细胞生长因子受体-2 (FGFR-2)的表达及其在胃黏膜癌变过程中的意义.方法:选择慢性浅表性胃炎(CSG)30例、胃黏膜肠上皮化生(IM)29例、不典型增生(Dys) 31例及胃癌(GC)55例.采用免疫组化SP法检测胃黏膜上皮细胞bFGF,FGFR-2表达状况,用快速尿素酶试验和组织学Warthin-Starry嗜银染色法联合检测胃黏膜H pylori感染情况.结果:CSG组bFGF,FGFR-2的表达显著低于其余三组(IM组:χ~2=4.002,P<0.05;χ~2= 4.163,P<0.05;Dys组:χ~2=15.779,P=0.000;χ~2=15.949,P=0.000;GC组:χ~2=24.110,P= 0.000;χ~2=18.736,P=0.000),IM组的表达低于Dys组及GC组(Dys组:χ~2=4.258,P<0.05;χ~2 =4.212,P<0.05:GC组:χ~2=7.786,P<0.01;χ~2 =4.687,P<0.05),而Dys组与GC组间无显著性差异.H pylori阳性IM及Dys组bFGF,FGFR-2的表达均显著高于阴性组(IM组:χ~2=10.076,P<0.01;χ~2=7.535,P<0.01;Dys组:χ~2=11.501,P<0.01;χ~2=8.330,P<0.01).H pylori阳性Dys组bFGF,FGFR-2表达显著高于GC组(χ~2= 4.201,P<0.05;χ~2=3.982,P<0.05),H pylori阳性IM组则与GC组的表达无显著性差异;H pylori阴性Dys组及IM组bFGF的表达均显著低于GC组(χ~2=5.736,P<0.05;χ~2=17.113,P= 0.000),H pylori阴性Dys组FGFR-2表达与GC组无显著性差异而IM组的FGFR-2的表达显著低于GC组(χ~2=11.091,P<0.05).结论:H pylori感染引起胃黏膜上皮细胞bFGF及FGFR-2的过度表达可能与H pylori感染致胃黏膜上皮细胞的癌变有关.     

胃幽门螺杆菌感染与抑癌基因失活的关系

目的探讨胃癌及癌前病变组织中幽门螺杆菌(H.pylori)感染与抑癌基因失活间的相互关系.方法运用DNA-PCR技术检测H.Pylori感染,采用PCR-RFLP,PCR-SSCP,RT-PCR及免疫组化技术分析182例胃癌及癌前病变及正常胃粘膜中抑癌基因APC,MCC,DCC,YNZ22及p53基因的杂合缺失、突变、mRNA及蛋白异常表达.结果胃癌及癌前病变组织中H.pylori的感染率(IM61.7%,Dys 63.3%,GC 42.3%)显著高于正常胃粘膜(17.5%,P＜0.05).但胃癌及癌前病变间H.pylori感染率无显著差别(P＞0.05),胃肠两型胃癌中H.pylori感染率分别为47.1%及42.2%,两者无显著差别(P＞0.05).胃癌及癌前病变组织中存在多种抑癌基因失活.H.pylori感染与癌前病变-肠化生中APC基因异常蛋白表达有关(Hp+43.2%vsHp-13.0%,P＜0.05).胃癌组织H.pylori感染阳性组中APC基因突变(50.0%)及蛋白表达(63.6%)、p53基因蛋白表达率(59.1%)显著高于阴性组(vs16.7%,P＜0.05;vs30.0%,P＜0.01;vs20.0%,P＜0.01).结论幽门螺杆菌感染及多种抑癌基因失活可能与胃癌的发生发展相关,H.pylori感染与APC,p53基因失活可能相关.     

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。     

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。     

c-Myc和端粒酶在幽门螺杆菌相关性胃病中协同表达

目的 通过检测幽门螺杆菌(Hp)相关性胃病[慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、异型增生及胃癌]中c—Myc和端粒酶的活性,分析c—Myc和端粒酶两者表达的关系,并探讨其与胃癌危险因子Hp之间的关系。方法 117例组织标本中c-Myc蛋白表达采用免疫组化法检测,端粒酶活性采用端粒酶PCR-ELISA法检测。结果 胃癌组中,端粒酶阳性率和c-Myc表达率(分别为87．7％和61．5％)高于非癌组;CAG伴有中、重度肠化组,端粒酶阳性率和c-Myc表达率(分别为52．4％和47．6％)显著高于CAG伴轻度肠化组(分别为13．3％和16．7％);有中、重度肠化的CAG组,伴有Hp感染者其端粒酶阳性率和c—Myc表达率(分别为67．9％和67．9％)显著高于无Hp感染者(分别为21．4％和7．1％);CSG组中无端粒酶阳性者。在胃癌及有中、重度肠化的CAG组,伴有Hp感染者其端粒酶阳性率和c—Myc表达率呈协同性增高(协同表达率分别为89．5％和100．0％)。结论 Hp感染可诱导慢性胃病、尤其是CAG中c-Myc和端粒酶的表达。在胃癌及CAG伴中、重度肠化的患者c-Myc和端粒酶协同表达。     

不同病变胃组织端粒酶活性及其与幽门螺杆菌感染的关系

目的:分析不同病变胃粘膜端粒酶活性的差异及其与幽门螺杆菌(H.Pylori)感染的关系,探讨端粒酶活性、H.pylori感染与胃粘膜癌变的关系.方法:应用端粒重复扩增法测定正常胃粘膜、癌前病变和胃癌组织中的端粒酶活性,用酶免疫法检测H.Pylori感染患者的血清H.Pylori-CagA-IgG水平,并分析端粒酶活性与H.Pylori-CagA-IgG水平的关系.结果:172例胃镜活检标本中,正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎无肠化、伴1度、2度肠化和胃癌组织的端粒酶阳性率分别为0%、0%、0%、25%、37.5%和88.89%.45例手术切除的胃癌组织和相应的非癌胃组织也呈相似结果.正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎无肠化及伴1度、2度肠化组织的H.pylori阳性率分别为0%、52.17%、60%、70%和75%.45例手术切除胃癌的非癌胃组织无肠化、伴1度、2度肠化的H.pylori感染强度分别为10.8±9.6个/50腺体、41.3±31.1个/50腺体和86.4±47.8个/50腺体.慢性浅表性胃炎患者的H.Py-lori-CagA-IgG抗体水平显著低于胃癌患者(P＜0.01),22例H.pylori阳性胃癌患者感染的H.pylori全部为cagA阳性菌株,其非癌胃粘膜有12例呈现端粒酶活性(54.55%);相反H.pylori阳性的22例慢性浅表性胃炎患者感染的H.Pylori只有8例为cagA阳性菌株(36.36%),其胃粘膜均未呈现端粒酶活性.结论:正常胃粘膜和浅表性胃炎不表达端粒酶活性,萎缩性胃炎的端粒酶活性随肠化进展而增高,胃癌组织中端粒酶活性最高,阳性率达88%以上.胃癌患者非癌胃粘膜中的端粒酶活性与肠化程度、H.Pylori感染强度呈平行关系,且感染的H.Pylori多为cagA阳性菌株;而慢性浅表性胃炎感染的H.pylori多为cagA阴性菌株.端粒酶活性检测可作为胃粘膜癌变的早期预测指标,cagA阳性的H.Pylori感染可能是端粒酶重新激活的启动信号.     

Helicobacter pylori infection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation

AIM: To investigate the relationship between Helicobacterpylori (H. pylori) infection and the expressions of the p53,Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseasesfrom chronic gastritis (CG), intestinal metaplasia type Ⅰ or Ⅱ(IMⅠ-Ⅱ), intestinal metaplasia type Ⅲ (IMⅢ), mild or modestdysplasia (DysⅠ-Ⅱ), severe dysplasia (DysⅢ) to gastric cancer(GC) and to elucidate the mechanism of gastriccarcinogenesis relating to H.pyloriinfection.METHODS: 272 cases between 1998 and 2001 wereavailable for the study including 42 cases of CG, 46 cases ofIMⅠ-Ⅱ, 25 cases of IMⅢ, 48 cases of DysⅠ-Ⅱ, 27 cases ofDysⅢ, 84 cases of GC.-H. pyloriinfection and the expressionsof p53, Rb, c-myc, bcl-2 were detected by means ofstreptavidin-peroxidase (SP) immunohistochemical method.HTERT mRNA was detected byin situ hybridization(ISH).RESULTS: The expressions of p53, Rb, c-myc, hTERT mRNAand bcl-2 were higher in the GC than in CG, IN, Dys. Theexpression of c-myc was higher in IMⅢ with-H.pyloriinfection(10/16) than that without infection (1/9) and the positive ratein DysⅠ-Ⅱ and DysⅢ with-H.pyloriinfection was 18/30 and 13/17, respectively, higher than that without infection (4/18 and3/10, respectively). In our experiment mutated p53 had noassociation with H.pyloriinfection, theexpression of Rb wasassociated with-H. pyloriinfection in GC, but the p53-Rb tumor-suppressor system abnormal in DysⅠ-Ⅱ cases, DysⅢⅡ and GCcases with H. pyloriinfection was 21/30, 15/17 and 48/48respecively, higher than non-infection groups (4/18, 3/10, 28/36). Furthermore the level of hTERT mRNA in GC with H. pyloriinfection (47/48) was higher than that without infection (30/36), however the relationship between bcl-2 and H. pyloriwasonly in IMⅢ. C-myc had a close association with hTERT mRNAin DysⅢ and GC (P＝0.0 253,0.0 305 respectively).CONCLUSION: In the gastric carcinogenesis, H. pylorimightcause the severe imbalance of proliferation and apoptosisin the precancerous lesions (IMⅢ and GysⅢ) first, leadingto p53-Rb tumor-suppressor system mutation and telomerasereactivation, and finally causes gastric cancer.     

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.     

幽门螺杆菌对GC及癌前病变抑癌基因和抑制细胞凋亡基因的影响

目的 探讨幽门螺杆菌(Hp)在胃癌(GC)和癌前病变中的作用及其与抑癌基因p53、抑制细胞凋亡基因Bcl-2表达的关系.方法 选取胃镜活检标本107例,其中GC28例,异型增生(DYS)14例,肠上皮化生(IM)16例,慢性萎缩性胃炎(CAG)34例,慢性浅表性胃炎(CSG)15例.尿素酶试验和Warthin-Starry银染色检测Hp,免疫组化SP法检测p53、Bcl-2基因蛋白的表达.结果 Hp感染阳性组中GC和癌前病变的发生率高于Hp感染阴性组(P<0.05),p53、Bcl-2的阳性表达率在GC、DYS和IM中明显高于CSG(P均<0.05).结论 Hp与GC发生关系密切,持续Hp感染所致的慢性炎症可引起胃黏膜损伤,促进了p53基因的突变和Bcl-2基因的表达.     

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。     

Anti-Helicobacter pylori immunoglobulin G （IgG） and IgA antibody responses and the value of clinical presentations in diagnosis of H.pylori infection in patients with precancerous lesions

AIM: To determine the prevalence of Helicobacter pylori(H. pylon) infection, the serum anti-H, pylori immunoglobulin G (IgG) and IgA antibody responses, and the value of clinical presentations in diagnosis of H. pylori infection in patients with gastric atrophy, intestinal metaplasia and dysplasia.METHODS: H. pylori infection was detected by histology in 209 patients with mild chronic atrophic gastritis (CAG, n=76),severe CAG (n=22), mild intestinal metaplasia (IM, n=22),severe IM (n=58), or dysplasia (DYS, n=31). Serum anti-H. pylori IgG and IgA were double sampled and evaluated by enzyme-linked immunoadsordent assays. 35 clinical presentations were observed and their relationship with H.pylori infection was analyzed by the k-means cluster method.RESULTS: Both IgG and IgA levels in H. pylori positive patients were significantly higher than those negative for H.pylori(P&lt;0.001-0.01). The prevalence of H. pyloriwas highest in severe IM (84.5%), and lowest in mild CAG (51.3%)(P&lt;0.01). They were similar in severe CAG (68.2%), mild IM (72.7%), and DYS (67.7%). In H. pyloripositive patients,the IgG levels in severe CAG were significantly higher than those in mild CAG (P&lt;0.01). In H. pylorinegative patients,both IgG and IgA levels increased remarkably in severe IM,compared to those in mild IM (P&lt;0.01-0.05). H. pyhri infection exhibited no association with patient‘s gender (62.1% inmales; 71.7% in females) and age (r=0.0814, P=0.241).The diagnostic accuracy based on 35 clinical presentations was 65.7%. It could be improved by 5.7% when only the assemblage of digestive symptoms were engaged, or by 8.6% when the pathogenic factors, general status and grossoscopy were combined. The diagnostic accuracy could be decreased when only the general symptoms were engaged, or when the pathogenic factors were accompanied with some common digestive symptoms.CONCLUSION: H. pylori infection is a major risk factor for the process from atrophy, IM to DYS of gastric mucosa.Serum IgG and IgA are good indicators to evaluate this progress with a certain arrearage. Investigation on the effective assemblages of clinical presentations may provide a better understanding in the pathogenesis, diagnosis and treatment for H. pyloriinfection.     

Roles of Helicobacter pylori infection and cyclooxygenase-2 expression in gastric carcinogenesis

AIM: Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach. METHODS: Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining. RESULTS: H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01). CONCLUSION: COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.     

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/     

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.     

幽门螺杆菌感染患者胃癌及癌旁组织中p53,p16和bc1—2基因的表达

研究幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ）感染胃癌得胃粘膜病变中抑癌基因ｐ５３、ｐ１６和关键性凋亡调节基因ｂｃ１－２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查ｐ５３、ｐ１６及ｂｃ１－２蛋白的表达。Ｈ．ｐｙｌｏｒｉ阳性由快速尿素酶试验结合病理染色／＾１     

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.     

Expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa

AIM: To investigate the expression of TFF2 and Helicobacter pyloriinfection in carcinogenesis of gastric mucosa.METHODS: The expression of TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 119 patients with endoscopic biopsy and subtotal gastrectomy specimens of gastric mucosal lesions, including 16 cases of chronic superficial gastritis (CSG), 20 chronic atrophic gastritis (CAG),35 intestinal metaplasia (IN), 23 gastric epithelial dysplasia (GED) and 25 gastric carcinoma (CA), and Helicobacter pylori infection was detected by Warthin-Starry staining.RESULTS: 1:TFF2 was located in the cytoplasm of gastrk mucous neck cell. The expression of TFF2 was 100 %,100 %, 0, 56.5 % and 0 in CSGs, CAGs, INs, GEDs and CAs, respectively. 2: The value of TFF2 positive cell density in CSG with Helicobacter pyloriinfection was higher than that without Helicobacter pyloriinfection. (52.89±7.27vs46.49±13.04, P＞0.05); But the value of TFF2 positive cell density in CAG and GED with Helicobacter pyloriinfection was significantly lower than that without Helicobacter pylori infection (18.17±4.09 vs 37.93±13.80, P＜0.01 and 14.44±9.32 vs 24.84±10.22, P＜0.05).CONCLUSION: Increase of TFF2 expression in CSG is perhaps associated with the protective mechanism after gastric mucosal injury. Decrease of TFF2 expression in CAG possibly attributes to the decrease in the number of gastric gland cell expressing TFF2. Re-expression of TFF2 in gastric epithelial dysplasia implies that TFF2 possibly contributes to the initiation of gastric carcinoma. The effect of Helicobacter pylori on the expression of TFF2 depends on the status of gastric mucosa.