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.     

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     

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/     

胃癌及癌前病变中bFGF FGFR-2及Hpa的表达及其意义

目的探讨胃癌及癌前病变中碱性成纤维细胞生长因子(bFGF)、成纤维细胞生长因子受体-2(FG-FR-2)及乙酰肝素酶(Hpa)的表达及其与胃癌发生发展的关系。方法选择广西医科大学第一附属医院2001—2005年手术切除和内镜活检的胃黏膜标本145例,其中慢性浅表性胃炎(CSG)组30例、胃黏膜肠上皮化生(IM)组29例、不典型增生(Dys)组31例、胃癌(GC)组55例,采用免疫组化SP法检测各组bFGF、FGFR-2及Hpa的表达。结果bFGF、FGFR-2的表达CSG组低于其余3组(P<0.05),IM组低于Dys组和GC组(P<0.05);Hpa在GC组表达显著高于其他3组(P<0.01);bFGF、FGFR-2及Hpa的表达与胃癌浸润深度、淋巴结转移、远处转移及TNM分期有关(P<0.01)。结论bFGF、FGFR-2及Hpa可能参与胃癌的发生发展过程,并可能加速胃癌的浸润和转移。     

Expression of COX-2 proteins in gastric mucosal lesions

AIM: To investigate the expression of COX-2 proteins in gastric mucosal lesions and to assess the relationship between COX-2 expression and type, pathologic stage, differentiation, or lymph node metastasis in gastric cancer and the relationship between COX-2 expression and H pylori infection in gastric mucosal lesions. METHODS: Thirty patients with gastric carcinoma underwent surgical resection. Samples were taken from tumor site and paracancerous tissues, and ABC immunohistochemical staining was used to detect the expression of COX-2 proteins. H pylori was determined by rapid urea test combined with pathological stating/14C urea breath test. RESULTS: The positive rate and staining intensity of mutant COX-2 gene expression in gastric cancer were significantly higher than those in paracancerous tissues (66.7% vs 26.7%) (P<0.01, P<0.001). There was a significant correlation between COX-2 and pathologic stage or lymph node metastasis type of gastric carcinoma (76.0% vs 20.0%, 79.2% vs 16.7%) (P<0.05). No correlation was found between COX-2 expression and type or grade of differentiation (P>0.05). COX-2 expression of intestinal metaplasia (IM) or dysplasia (DYS) with positive H pylori was significantly higher than that with negative H pylori (50.6% vs 18.1%, 60.0% vs 33.3%) (P<0.05). CONCLUSION: COX-2 overexpression was found in a large proportion of gastric cancer tissues compared with matched non-cancerous tissues and was significantly associated with advanced tumor stage and lymph node metastasis. Overexpression of COX-2 plays an important role in tumor progression of gastric cancer. COX-2 may also play a role in the early development/promotion of gastric carcinoma and is associated with H pylori infection.     

幽门螺杆菌感染诱导胃粘膜环氧化酶-2表达

目的 探讨幽门螺杆菌（Hp)感染对胃粘膜环氧化酶－2（COX－2）表达的影响。方法 27例无任何症状健康检查者，经胃镜采取胃窦部粘膜组织，用于Hp检测、病理组织学检查及免疫组织化学检查COX－2的表达。结果 18例Hp感染者胃粘膜上皮细胞和炎症细胞表达COX－2，而9例Hp阴性者胃粘膜均不表达COX－2。结论 Hp感染诱导胃粘膜COX－2表达。     

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.     

环氧合酶-2表达与幽门螺杆菌相关性胃十二指肠疾病的研究

目的　探讨环氧合酶 2表达与幽门螺杆菌Helicobacterpylori ,H .pylori相关性胃十二指肠疾病的关系 ,并通过抗菌治疗评价根除H pylori感染对胃窦黏膜中COX 2表达的影响。方法　用免疫组化方法半定量检测 2 64例经胃镜和组织病理学检查患有十二指肠球部溃疡、胃溃疡、复合性溃疡、胃癌、单纯性慢性胃炎及胃黏膜正常者的胃窦黏膜COX 2蛋白的表达 ,比较H pylori感染与非感染者之间的差异。对检出的 3 5例H pylori的单纯慢性胃炎进行H pylori抗菌根除治疗 ,比较根除前后胃窦黏膜COX 2蛋白的表达变化。根据 2 0 0 0年 5月全国慢性胃炎研讨会共识意见 (江西 井冈山 )对胃黏膜炎症、活动性、异型增生、肠化生和H pylori密 ,度进行半定量测定。结果　胃黏膜表面上皮、腺上皮细胞和固有层间质细胞的浆中可见COX 2蛋白表达 ,但阳性染色细胞多集中在表层上皮。 2 53例中 ,14 3例H pylori者 (56 52 % )COX 2平均阳性细胞率显著高于 110例H pylori者 (43 48% ) ,(P =0 ) ,各疾病组H pylori患者的COX 2平均阳性细胞率均显著高于H pylori者 (P =0 ) ,各疾病组H pylori患者COX 2平均阳性细胞率也均显著高于正常对照组 (P <0 0 5)。 2 7例H pylori根除后的胃黏膜COX 2平均阳性细胞率明显下降 (P =0 ) ,但仍明显高于正     

Role of intestinal metaplasia subtyping in the risk of gastric cancer in Korea

Background and Aim:  Gastric cancer is believed to develop by a multistage process. Intestinal metaplasia (IM) is regarded as a premalignant condition; it is classified into subtypes I, II and III. The aim of this study was to evaluate whether the subtypes of IM were associated with progression to gastric cancer.
Methods:  The study cohort consisted of 861 subjects, categorized as controls, gastric ulcers, dysplasia and cancer. The IM was scored histologically using the Sydney classification for the antrum and the body of the stomach. The biopsies were stained with high iron diamine and alcian blue (pH 2.5) (HID-AB2.5), and the IM was subtyped as I, II or III.
Results:  The proportion of IM subtypes I, II and III were 14.5%, 47.2% and 38.3% in the antrum, and 28.1%, 57.8% and 14.1% in the body of the stomach, respectively. These distributions did not show significant differences depending on disease or Helicobacter pylori positivity. In cases that were H. pylori -positive, the prevalence of IM subtype II in the cancer and dysplasia groups was higher than in the control group in the body of the stomach ( P  < 0.05). The proportion of IM subtype III in the antrum increased in proportion with age ( P  = 0.036).
Conclusions:  IM subtyping was not found to play a major role in the prediction of gastric cancer development in Korea. IM subtype III was associated with aging, and IM subtype II appeared to be related to gastric carcinogenesis in the presence of H. pylori infection.     

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.     

幽门螺杆菌相关胃疾病组织中P53、iNOS的表达

目的通过检测慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、胃癌组织幽门螺杆菌（Hp）和P53、一氧化氮合成酶（iNOS），探讨Hp感染与P53、iNOS表达的关系，以及Hp感染导致胃癌的可能分子机制。方法应用快速尿素酶试验和组织切片革兰氏染色和血清HpCagA抗体检测Hp，用免疫组化SP法检测上述组织的P53、iNOS。结果慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、胃癌组织中Hp检出率分别为45．9％、68．4％、71．4％、75．O％、54．8％，病变各组中P53和iNOS表达阳性率与浅表性胃炎组比较均有显著性差异。除浅表性胃炎组、萎缩性胃炎Hp阳性组的P53表达阳性率外，各病变Hp阳性组的P53和iNOS表达阳性率与各组的Hp感染阳性率呈正相关，各病变组中Hp（＋）组的P53和iNOS表达阳性率显著高于Hp（-）组，均有显著性差异。结论Hp与P53和iNOS阳性表达有一定的相关性。     

Intracellular and interstitial expression of Helicobacter pylori virulence genes in gastric precancerous intestinal metaplasia and adenocarcinoma

Gastric intestinal metaplasia (IM) and gastric cancer are associated with Helicobacter pylori, but the bacterium often is undetectable in these lesions. To unravel this apparent paradox, IM, H. pylori presence, and the expression of H. pylori virulence genes were quantified concurrently using histologic testing, in situ hybridization, and immunohistochemistry. H. pylori was detected inside metaplastic, dysplastic, and neoplastic epithelial cells, and cagA and babA2 expression was colocalized. Importantly, expression of cagA was significantly higher in patients with IM and adenocarcinoma than in control subjects. The preneoplastic "acidic" MUC2 mucin was detected only in the presence of H. pylori, and MUC2 expression was higher in patients with IM, dysplasia, and cancer. These novel findings are compatible with the hypothesis that all stages of gastric carcinogenesis are fostered by persistent intracellular expression of H. pylori virulence genes, especially cagA inside MUC2-producing precancerous gastric cells and pleomorphic cancer cells.     

胃癌和癌前病变中幽门螺杆菌及环氧化酶-2和p53的表达及相关性研究

[目的]检测慢性胃炎、胃癌前病变及胃癌（GGa）的胃黏膜组织中幽门螺杆菌（Hp）,环氧化酶-2（COX-2）和突变型p53的表达,探讨Hp感染在胃癌发生过程中与COX-2、p53动态表达的相关性.[方法]选择经胃镜检查及病理组织学证实为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、肠上皮化生（IM）、不典型增生（Dys）及GCa患者各100例,快速尿素酶试验（HPUT法）和组织学改良Giemsa染色联合检测Hp,通过免疫组化检测Hp感染组和非感染组患者胃黏膜COX-2、p53.[结果]①Hp、COX-2阳性率随病变进展呈上升趋势,Hp阳性率在CAG、IM、Dys、GCa各组中显著高于CSG组（P＜0.05）;COX-2在IM、Dys、GCa各组中与慢性胃炎比较有统计学意义（P＜0.05）;②Hp感染阳性率和COX-2蛋白表达阳性率在胃癌前病变组织中存在相关性（P＜0.05）;③p53阳性率在GCa与CSG、CAG相比差异有统计学意义（P＜0.01）;④在GCa组中,Hp阳性组p53的阳性表达明显高于Hp阴性组（P＜0.05）.[结论]GCa的形成与Hp感染、突变型p53、COX-2等多种因素及其相互作用有关,可视为GCa发生的危险预警信号之一;在GCa高危人群的追踪观察和随访中,进行Hp、p53、COX-2的联合检测,对发现胃癌前病变和GCa有一定临床意义.     

Microsatellite instability in gastric cancer and pre-cancerous lesions

AIM: To investigate the microsatellite instability (MSI) in cancer and pre-cancerous lesions of the stomach and its mechanisms underlying the development of gastric cancer. METHODS: Thirty-six gastric cancer samples were obtained from patients undergoing surgery. Forty-one gastric mucosa samples with dysplasia and 51 with intestinal metaplasia (IM) were obtained from patients with chronic gastritis undergoing gastro-endoscopy. Genomic DNA was extracted from the samples. Silver staining single strand conformation polymorphis-polymerize chain reaction (SSCP-PCR) was used to screen MSI markers at 5 loci (Bat-25, Bat-26, D5S346, D17S250, and D2S123) in fresh tissues and formalin-fixed, paraffin-embedded samples and their corresponding normal gastric mucosa. RESULTS: The abnormal shifting of the single-strand DNA (MSI) was identified in 21 out of 36 (58.3%) gastric cancers. Seven cases showed high-level MSI (two or more loci altered) and 14 showed low-level MSI (one locus altered). Gastric cancer with MSI had a tendency to be located in the distal stomach. MSI was also detected in 11 out of 41 (26.8%) dysplasia samples and in 9 of 51 (17.6%) IM samples respectively. Three cases of dysplasia and one case of IM showed high-level MSI. Eight cases of dysplasia and 8 cases of IM displayed low-level MSI. MIS in IM was found only in moderate or severe-grade IM. No association was detected between MSI and dysplasia grade. CONCLUSION: Accumulation of MSI in dysplasia and intestinal metaplasia of gastric mucosa may be an early molecular event during gastric carcinogenesis and may contribute to the acquisition of transformed cell phenotype and the development of gastric cancer.     

胃粘膜肠化与幽门螺杆菌分布的关系

目的：探讨胃癌高发地区人群中胃粘膜肠化与幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ）分布的关系。方法：对５３３例胃癌高发地区成年人行内镜及胃粘膜活检组织学检查,Ｗａｒｔｈｉｎ－Ｓｔａｒｒｙ染色阳性定为Ｈ．ｐｙｌｏｒｉ感染。结果：５３３例成年人的Ｈ．ｐｙｌｏｒｉ检出率为６４．５％。Ｈ．ｐｙｌｏｒｉ阳性组肠化检出率为５５．５％,阴性组肠化检出率为３１．８％（Ｐ〈０．０１）。Ｈ．ｐｙｌｏｒｉ阳性组无肠化和轻、中、重度     

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。     

Correlations among Helicobacter pylori infection and the expression of cyclooxygenase‐2 and vascular endothelial growth factor in gastric mucosa with intestinal metaplasia or dysplasia

Background and Aims: To examine the rate of Helicobacter pylori infection and the expression of cyclooxygenase‐2 (COX‐2) and vascular endothelial growth factor (VEGF) in gastric mucosa with intestinal metaplasia or dysplasia, and explore their correlations in precancerous gastric lesions. Methods: A total of 172 patients were included in the study. H. pylori infection was evaluated by hematoxylin–eosin and modified Giemsa staining. The expression of COX‐2 and VEGF proteins was detected by immunohistochemistry. Results: The rates of H. pylori infection in gastric mucosal dysplasia (DYS), intestinal metaplasia in gastric mucosa (IM), chronic atrophic gastritis (CAG) and chronic superficial gastritis (CSG) patients were significant differences (P = 0.001). The average optical density (AOD) values of COX‐2 staining in CSG, CAG, IM and DYS patients were 13.81 ± 5.53, 45.28 ± 21.44, 73.67 ± 26.02 and 91.23 ± 45.11, respectively, with significant differences among CSG, CAG and IM patients (P = 0.037, 0.001 and 0.047 for CSG vs CAG, CSG vs IM and CAG vs IM, respectively). The expression level of VEGF in DYS patients was significantly higher than those in other patients (P = 0.001, 0.001 and 0.001 for DYS vs CSG, DYS vs CAG and DYS vs IM, respectively). The expression levels of COX‐2 in H. pylori‐positive IM, CAG and DYS patients were significantly higher than those in H. pylori‐negative counterparts (P = 0.043, 0.009, 0.001, respectively). Additionally, the expression level of COX‐2 was positively correlated with that of VEGF with the aggravation of gastric mucosal lesions (r = 0.640, P = 0.006). Conclusion: H. pylori infection might be able to induce the expression of COX‐2 in precancerous gastric lesions, which in turn upregulates the expression of VEGF.     

胃黏膜细胞线粒体DNA不稳定及核内整合与幽门螺杆菌感染有关

目的：线粒体DNA（mtDNA）因缺乏组蛋白保护，且损伤修复系统不健全，容易为幽门螺杆菌（Hp）相关胃炎中氧自由基的重要靶点，为此探讨胃黏膜细胞线粒体DNA不稳及核内整合与Hp感染的关系。方法：采用PCR和Giemsa染色检测Hp；采用限制性片段多态性（PCR－SSCP）和原位杂交方法检测胃黏膜细胞线粒体DNA微卫星不稳定（mtMSI）及核内mtDNA序列。结果：30例胃癌检出mtMSI11例（36．7％），15例肠化中有2例（13．3％），10例异型增生中有2例，10例萎缩性胃炎中有1例检出mtMSI。胃癌细胞核内mtDNA序列的检出率为20．0％（6／30），异型增生为1／10例，肠上皮化生为6．7％（1／15），萎缩性胃炎为1／10例，胃黏膜细胞mtMSI及核内mtDNA序列的检出率在Hp感染组（12／39，8／39）显著高于非Hp感染组（4／36，1／36，P＜0．05）。虽cagA^ 组mtMSI及核内mtDNA序列检出率（10／25，6／25）高于cagA^-组（2／14，2／14），但两组mtMSI及核内mtDNA序列检出率比较，差异并无显著性（P＞0．05）。结论：胃黏膜细胞mtMSI及mtDNA序列核内整合可能与Hp感染有关，并参与胃癌的发生。     

Expression of ornithine decarboxylase in precancerous and cancerous gastric lesions

AIM: To investigate the expression of ornithine decarboxylase (ODC) in precancerous and cancerous gastric lesions. METHODS: We studied the expression of ODC in gastric mucosa from patients with chronic superficial gastritis (CSG,n = 32),chronic atrophic gastritis CAG,n = 43; 15 with and 28 without intestinal metaplasia (IM),gastric dysplasia (DYS,n = 11) and gastric cancer (GC,n = 48) tissues using immunohistochemical staining. All 134 biopsy specimens of gastric mucosa were collected by gastroscopy. METHODS: The positive rate of ODC expression was 34.4%,42.9%,73.3%,81.8% and 91.7% in cases with CSG,CAG without IM,CAG with IM,DYS and GC,respectively (P < 0.01),The positive rate of ODC expression increased in the order of CSG < CAG (without IM) < CAG (with IM) < DYS and finally,GC. In addition,ODC positive immunostaining rate was lower in well-differentiated GC than in poorly-differentiated GC (P < 0.05). CONCLUSION: The expression of ODC is positively correlated with the degree of malignity of gastric mucosa and development of gastric lesions. This finding indicates that ODC may be used as a good biomarker in the screening and diagnosis of precancerous lesions.