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1.
目的 检测TGF-β1、TGF-βRⅡ、Smad2/3及CDC25蛋白在胃癌组织中的表达并探讨它们在胃癌组织中的发生、发展的意义.方法 利用免疫组织化学SP法检测110例胃癌、21例高级别上皮内瘤变、17例低级别上皮内瘤变、54例肠上皮化生、28例慢性萎缩性胃炎和57例正常胃黏膜组织中TGF-β1、TGF-βRⅡ、Smad2/3和CDC25蛋白的表达.结果 TGF-β1、TGF-βRⅡ、Smad2/3和CDC25在胃癌组织中的表达均高于正常胃黏膜组织.TGF-β1在胃癌组织中的表达高于上皮内瘤变、肠上皮化生和慢性萎缩性胃炎组织;Smad2/3在胃癌组织中的表达高于慢性萎缩性胃炎组织;CDC25在胃癌组织中的表达高于低级别上皮内瘤变组织,且在胃癌淋巴结转移组中的表达高于未转移组.TGF-β1与TGF-βRⅡ、Smad2/3和CDC25呈正相关,Smad2/3与CDC25也呈正相关.结论 TGF-β1、TGF-βRⅡ、Smad2/3和CDC25的表达是引起胃癌发生、发展的重要因素,可作为胃癌早期诊断的辅助指标.  相似文献   

2.
目的 通过人雄激素受体基因位点克隆性分析技术对胃癌及其癌前病变进行克隆性分析,探讨胃癌发生发展过程中单克隆发生率的变化趋势及与Ki-67表达之间的关系及其意义.方法 肠型胃癌根治标本24例,胃镜活检标本150例.采用激光显微切割技术准确获取病变腺上皮细胞,基因组DNA经甲基化敏感的Hpa Ⅱ限制性内切酶消化后,PCR扩增人雄激素受体基因,采用基因扫描技术对PCR产物进行分析.应用免疫组织化学EnVision二步法检测Ki-67在以上病变组织中的表达,并探讨其与克隆性分析结果的相关性.结果 单克隆发生率在胃黏膜肠上皮化生(15.63%,5/32)、低级别上皮内瘤变(22.22%,10/45)、高级别上皮内瘤变(69.44%,25/36)及肠型胃癌(100.0%,20/20)中逐渐增加,除胃黏膜肠上皮化生和低级别上皮内瘤变之间的差异没有统计学意义(P=0.47),其他各组之间差异均有统计学意义(P<0.01).Ki-67的阳性表达率随着病变的发展而不断升高.低级别上皮内瘤变组织中单克隆病例的Ki-67的阳性表达率显著高于多克隆病例(P<0.01),且克隆性与Ki-67的阳性表达率之间存在显著相关性(P<0.01).结论 单克隆的发生率及Ki-67的阳性表达率在胃癌发生发展过程中逐渐增加.且单克隆病变的发生与Ki-67的表达存在一定的相关性,两者的联合可用于胃癌的早期诊断及易感性的预测.  相似文献   

3.
目的探讨EZH2和p53蛋白在胃癌组织中的表达,及其在胃癌发生、发展过程中的作用和临床病理学意义。方法采用免疫组化EnVision法检测EZH2和p53蛋白在199例胃癌、25例高级别上皮内瘤变、24例低级别上皮内瘤变、46例肠上皮化生、17例慢性萎缩性胃炎和23例正常胃黏膜组织中的表达情况。结果在胃癌和上皮内瘤变组织中EZH2蛋白表达明显高于肠上皮化生、慢性萎缩性胃炎和正常胃黏膜组织。胃癌组织中EZH2蛋白的表达在进展期胃癌高于早期胃癌,差异有统计学意义。EZH2蛋白在胃癌组织中的表达与肿瘤的大小、淋巴结转移、组织学分期和临床分期均有关;但与患者的性别、年龄、肿瘤的部位、肿瘤的类型和分化以及患者的病死率均无关。p53蛋白在胃癌组织中表达最高,几乎不表达于其他病变和正常胃黏膜组织。p53表达水平与患者的年龄、性别、肿瘤大小、淋巴结转移、肿瘤分化、胃癌的类型和患者的生存情况相关。EZH2蛋白表达与p53蛋白表达之间呈正相关。结论 EZH2在胃癌中的表达增加与p53相关,提示胃癌中EZH2与p53可能相互协调,促进胃癌的发生、发展。  相似文献   

4.
胃癌及癌前病变组织中VEGF和iNOS蛋白的表达   总被引:1,自引:0,他引:1  
目的:观察胃癌及癌前病变(肠上皮化生、不典型增生)组织中血管内皮细胞生长因子(VEGF)和诱导型一氧化氮合酶(iNOS)的表达,探讨其临床意义。方法:选择我院2008-01/2010-01手术切除和内镜活检的胃黏膜标本150例,其中胃黏膜肠上皮化生组50例,不典型增生组50例,胃癌组50例;另40例来自胃镜胃黏膜活检的正常胃黏膜标本作为对照组。免疫组化染色法比较各组VEGF和iNOS的表达。结果:胃癌组VEGF和iNOS的表达高于其余3组(P<0.01);肠上皮化生组与不典型增生组的表达无显著差异;但均明显高于对照组(P<0.05)。结论:胃镜黏膜组织活检VEGF和iNOS的表达与组织恶变程度相关,有利于胃癌的早期诊断。  相似文献   

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目的 探讨IGFBP-4(insulin-like growth-factor-binding proteins-4)蛋白在胃癌发生、发展中的作用.方法 采用免疫组化SP法分别检测正常胃黏膜、胃上皮内瘤变和胃癌组织中IGFBP-4蛋白的表达.结果 20例正常胃黏膜组织中IGFBP-4蛋白阳性率为10%,胃上皮内瘤变组织中的阳性率为36.84%,胃癌组织中的阳性率为81.25%;胃癌组织中IGFBP-4蛋白表达高于胃上皮内瘤变及正常胃黏膜组织(P<0.001),胃上皮内瘤变与正常胃黏膜的差异有显著性(P<0.05);高分化胃癌中IGFBP-4蛋白阳性率为57.14%,低分化胃癌中的阳性率为88.4%,两者之间差异有显著性(P<0.05);早期胃癌阳性率为55.0%,明显低于进展期胃癌86.96%;伴淋巴结转移组阳性率为89.04%,无淋巴结转移组阳性率为66.67%,差异有显著性;而与性别、年龄、肿瘤直径无关.结论 IGFBP-4蛋白的高表达与胃癌的发生、淋巴结转移及临床分期相关.  相似文献   

6.
目的 观察Ataxin-3蛋白在人胃癌组织中的表达及分布,探讨其在胃癌发生、发展过程中的意义及与临床病理学特征的关系.方法 采用免疫组化SuperVision两步法检测Ataxin-3在胃癌(265例)、正常胃黏膜(209例)、胃低级别上皮内瘤变(86例)及高级别上皮内瘤变(75例)组织中的表达,并对其表达与临床病理学特征的关系进行统计学分析.结果 Ataxin-3的表达,在胃癌组织中低于正常胃黏膜组织(P<0.001);胃癌组与低级别上皮内瘤变组中的表达有差异(P﹤0.001),而胃癌组与高级别上皮内瘤变组比较表达无差异(P>0.05);Ataxin-3表达与胃癌的Lauren组织学分型、肿瘤分化、远处转移及p53突变蛋白的表达存在相关性(P均<0.05).结论 Ataxin-3蛋白很可能在胃癌的发生、发展过程中起重要意义.  相似文献   

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目的:探讨慢性萎缩性胃炎患者幽门螺旋杆菌感染与胃黏膜中转化生长因子茁受体域、白介素6 和肿瘤坏死因子琢的表达情况。方法:选取76例慢性萎缩性胃炎(CAG)患者胃黏膜病变组织的胃镜活检标本,采取PCR 荧光法检测Hp 感染情况,免疫组化法检测TGF-βRⅡ、IL-6 和TNF-α在胃小凹上皮和间质炎细胞中的表达。结果:慢性炎症程度在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);间质炎细胞中IL-6的表达在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);TGF-βRⅡ、TNF-α的表达在Hp感染阳性组和阴性组中无显著性差异(P>0.05);间质炎细胞中IL-6与慢性炎症程度呈正相关关系(r=0.249,P=0.03);萎缩程度与肠上皮化生严重程度、上皮内瘤变程度呈正相关关系(r=0.697,0.366)。结论:IL-6在间质炎性细胞中的表达与Hp相关性CAG患者的慢性炎症程度有关,慢性萎缩程度促进肠上皮化生和上皮内瘤变的发生。  相似文献   

8.
目的:探讨慢性萎缩性胃炎患者幽门螺旋杆菌感染与胃黏膜中转化生长因子β受体Ⅱ、白介素6和肿瘤坏死因子α的表达情况。方法:选取76例慢性萎缩性胃炎(CAG)患者胃黏膜病变组织的胃镜活检标本,采取PCR荧光法检测Hp感染情况,免疫组化法检测TGF-βRⅡ、IL-6和TNF-α在胃小凹上皮和间质炎细胞中的表达。结果:慢性炎症程度在Hp感染阳性组和阴性组中差异有统计学意义(P0.05);间质炎细胞中IL-6的表达在Hp感染阳性组和阴性组中差异有统计学意义(P0.05);TGF-βRⅡ、TNF-α的表达在Hp感染阳性组和阴性组中无显著性差异(P0.05);间质炎细胞中IL-6与慢性炎症程度呈正相关关系(r=0.249,P=0.03);萎缩程度与肠上皮化生严重程度、上皮内瘤变程度呈正相关关系(r=0.697,0.366)。结论:IL-6在间质炎性细胞中的表达与Hp相关性CAG患者的慢性炎症程度有关,慢性萎缩程度促进肠上皮化生和上皮内瘤变的发生。  相似文献   

9.
Ki-67在胃癌及癌旁组织中的表达   总被引:1,自引:0,他引:1  
孙希印  高虹 《解剖与临床》2003,8(4):215-216
目的:探讨Ki-67在胃癌和癌旁黏膜上皮中的表达、分布特征及其在胃癌组织发生学上的意义。方法:采用免疫组化方法对36例胃癌及癌旁组织进行检测。结果:胃腺癌与癌旁伴异型增生慢性萎缩性胃炎Ki-67阳性率无显著性差异;胃腺癌与癌旁伴高、中增殖型肠上皮化生慢性萎缩性胃炎Ki-67阳性率无显著性差异(P>0.05)。结论:Ki-67是一种较好的癌前标志物,胃黏膜上皮异型增生和高、中增殖型肠上皮化生萎缩性胃炎与胃癌的发生密切相关。  相似文献   

10.
目的: 探讨环氧合酶-2 (COX-2)和C-met蛋白在胃黏膜癌变过程中的变化规律及其意义.方法:采用Envision法,用20例慢性浅表性胃炎作为对照组,对38例慢性萎缩性胃炎伴肠上皮化生、38例肠化伴异型增生和76例胃腺癌标本,分别检测COX-2和C-met蛋白的表达情况,并分析其间的相关性.结果: C-met蛋白在慢性浅表性胃炎组的表达低于其他胃黏膜病变组织;从非萎缩性胃炎胃黏膜组织→肠化生→异型增生→胃癌,COX-2的表达逐渐增高.COX-2与C-met蛋白的表达呈正相关.结论: 细胞增殖和凋亡相关因子C-met蛋白与COX-2表达异常在胃黏膜癌变过程中发挥重要作用.  相似文献   

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N. ECTORS  M.F. DIXON 《Histopathology》1986,10(12):1271-1277
Gastric biopsy specimens from 230 patients with chronic atrophic gastritis were investigated with the use of mucin stains for the presence and type of intestinal metaplasia. Metaplasia was not shown in 59 cases; 92 of the 171 cases with metaplasia were sulphomucin positive and 79 were negative. The patients were followed-up from 1976 to 1985. Eight patients were registered as having gastric cancer over this period. However, five of them had to be eliminated from the study because on careful review of all the clinical data it was clear that they had gastric cancer at the time of the biopsy. Two of the three remaining patients had sulphomucin negative biopsies. Thus, only one patient out of 90 with chronic atrophic gastritis and sulphomucin positive intestinal metaplasia developed gastric cancer when followed-up for 8-9 years. None of the patients with unequivocal type IIb metaplasia developed gastric cancer. We conclude that sulphomucin positive intestinal metaplasia does not identify a high risk group and its recognition is thus of no value in surveillance for gastric cancer.  相似文献   

14.
Lewis (Le)-associated antigens are carbohydrates that are related biochemically to the ABO blood groups, and may have a role in Helicobacter pylori adherence. To evaluate their relationship to clinicopathological outcomes, gastric Le expression, including type 1 precursor, type 1 H, Le(a), Le(b), Le(x), Le(y) and sialylated Le(a) (CA19-9), was evaluated immunohistochemically in 233 gastric biopsy specimens obtained at routine gastroscopy. Expression was also investigated in gastric tissues showing chronic gastritis, intestinal metaplasia, and carcinoma from 42 patients with gastric cancer. A polymerase chain reaction was performed for H. pylori and the bacterial babA2 gene. We identified type 1 precursor expression in 34.3%, type 1 H in 55.8%, Le(a) in 44.2%, Le(b) in 82.0%, Le(x) in 44.2%, Le(y) 56.7%, and CA19-9 in 16.3% of the 233 gastric biopsy specimens. Expression of type 1 H, Le(b), and CA19-9 was significantly associated with H. pylori infection and histological features (p < 0.05), and expression of type 1 H was an independent predictive factor for H. pylori infection by multivariate logistic regression (p = 0.020). Positivity for the babA2 genotype correlated significantly with H. pylori infection and type 1 H expression in gastric biopsy specimens (p < 0.05). The babA2 genotype was more frequent in gastric mucosa from the gastric cancer patients than in gastric biopsy specimens from routine gastroscopy (p = 0.009). In the 42 gastric cancer patients, the frequency of type 1 precursor, Le(a), and Le(x) expression was significantly higher in intestinal metaplasia and carcinoma than in chronic gastritis (p < 0.05), but the frequency of type 1 H and Le(b) expression was significantly lower in intestinal metaplasia and carcinoma (p < 0.05). In conclusion, Le expression, especially that of type 1 H, was significantly associated with clinicopathological features. In gastric cancer patients, Le expression was altered in intestinal metaplasia and carcinoma in comparison with chronic gastritis.  相似文献   

15.
Objective: To investigated the influence of H. pylori on TLR4 and TLR9 in gastric mucosa during gastric carcinogenesis. Methods: Gastric biopsy specimens were taken from 148 patients and divided into five groups, including normal group (n = 10), chronic superficial gastritis group (n = 35), atrophy/intestinal metaplasia group (n = 35), dysplasia group (n = 34) and gastric carcinoma group (n = 34). Immunohistochemistry was used to detect the expression of TLR4 and TLR9. Geimsa staining and rapid urea test were used for determine H. pylori infection. Results: TLR4 was detected in gastric epithelium and monocytes/macrophages in superficial gastritis, atrophy/intestinal metaplasia, dysplasia or carcinoma. TLR9 was mainly accentuated in monocytes/macrophages. TLR4 positive cells in epithelium and in monocytes/macrophages with H. pylori infection were much more than those without H. pylori infection. Similar results were also found in TLR9. When gastric epithelium was accompanied with H. pylori infection, TLR4 was significant higher in superficial gastritis and atrophy/intestinal metaplasia groups compared with dysplasia and carcinoma groups. When gastric epithelium was infected by H. pylori, TLR9 was significant higher in carcinoma group compared with superficial gastritis, atrophy/intestinal metaplasia and dysplasia. TLR4 and TLR9 show significant correlation with the severity of inflammation. Conclusions: H. pylori infection was associated with increased expression of TLR4 and TLR9 in gastric mucosa. In superficial gastritis and atrophy/intestinal metaplasia the inflammation was predominately mediated by TLR4, while in gastric cancer the inflammation was mainly mediated by TLR9.  相似文献   

16.
c-met蛋白表达与胃粘膜病变的关系及预后意义   总被引:5,自引:0,他引:5  
目的 研究c-met蛋白在胃粘膜病变演进过程中的表达及关系,探讨c-met表达对胃癌预后的意义。方法 对169例经病理证实的不同胃粘膜病变采用免疫组织化学SP法检测c-met蛋白表达,用Kaplan-Meier法的Log-rank检验胃癌生存率。结果 在浅表性胃炎、萎缩性胃炎、肠化生、异型增生、早期胃癌和进展期胃癌中,c-met蛋白表达率分别为23.5%(4/17),36.8%(14/38),51.5%(17/33),61.3%(19/31),66.7%(8/12)和73.7%(28/38),而且肠化生、异型增生、胃癌均显著高于浅表性胃炎(P〈0.05)。胃粘膜增殖程度与c-met阳性表达强度密切关系分析,两者有显著关联(P〈0.01)。c-met阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关,而且Bor  相似文献   

17.
AIMS: The causal relationship of H. pylori gastric colonization with gastric cancer development has not as yet been fully elucidated. The prevalence of H. pylori infection increases with age in the asymptomatic population in Japan, and reaches a high plateau in those older than 40 years. The objective of this study was to assess the link between H. pylori and gastric carcinomas in patients younger than 40 years. METHODS AND RESULTS: Detection of H. pylori and assessment of background mucosa based on the Sydney system was performed histopathologically for 40 Japanese gastric cancer cases younger than 40 years and compared with 40 age- and sex-matched controls. H. pylori infection in gastric mucosa was detected significantly more frequently (P < 0.001) in patients with cancer (29/40; 72.5%) than in controls (11/40; 27.5%). Additionally, by histopathological comparison between intestinal (18 cases) and diffuse (70 cases) types of young gastric cancer patients, mucosal atrophy and intestinal metaplasia were found to coexist with acute and chronic inflammation in the background mucosa of both intestinal and diffuse types, being significantly more prevalent than in young controls. CONCLUSIONS: As well as the high prevalence of H. pylori in young subjects with gastric cancer, it is clear that persistent infection induces mucosal damage, resulting in atrophy and intestinal metaplasia. Thus, acute/chronic gastritis could play an essential role in the early development of neoplasia in the stomach.  相似文献   

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Intestinal metaplasia is a key event in multistep gastric carcinogenesis. CDX2, a master regulator of intestinal phenotype, was shown to play a tumor-suppressive role in colon cancer. However, it was reported to be expressed in nearly all gastric intestinal metaplasia and many gastric cancers. As CDX2 is differentially expressed in normal stomach and intestine, we sought to relate the CDX2 expression to gastrointestinal differentiation along gastric carcinogenesis. The expression of CDX2 protein in gastric intestinal metaplasia, dysplasia and cancer was examined and related to their gastrointestinal differentiation. CDX2 expression was significantly decreased in incomplete intestinal metaplasia, which expresses both gastric mucins (MUC5AC and MUC6) and intestinal mucin (MUC2), compared with complete intestinal metaplasia, which expresses intestinal mucin (MUC2) only. Although incomplete intestinal metaplasia morphologically resembles colon, its CDX2 expression was apparently lower than that in the normal colon. Moreover, CDX2 expression was progressively reduced in gastric dysplasia and cancer. The CDX2 expression in gastric cancer was also inversely correlated with the expression of gastric mucins. As incomplete intestinal metaplasia is associated with higher risk of gastric cancer, its lower CDX2 expression compared with that in complete intestinal metaplasia and normal colon epithelium resolved the current contradiction between the tumor-suppressive role of CDX2 in the colon and the high prevalence of CDX2 in intestinal metaplasia. Further decrease of CDX2 expression in gastric dysplasia and cancer suggests that CDX2 plays a similar anticarcinogenic role in intestinal metaplasia as it does in colon. Intestinal metaplasia or dysplasia with low expression of CDX2 may serve as predictive markers for gastric cancer.  相似文献   

19.
目的 探讨胃、肠免疫表型标志物在早期胃印戒细胞癌中的表达及其与临床病理参数和预后的相关性.方法 免疫组织化学EnVision法检测91例早期胃印戒细胞癌中胃免疫表型标志物MUCI、MUCSAC、MUC6和肠免疫表型标志物MUC2、CDX2的表达,并根据肿瘤细胞胃、肠免疫表型标志物表达水平的差异,将早期胃印戒细胞癌分为3种类型:胃型、肠型和混合型.结果 胃型、混合型和肠型印戒细胞癌分别为53例(58.2%)、22例(24.2%)和16例(17.6%).胃、肠免疫表型标志物表达水平与印戒细胞癌形态学分型无相关性(P>0.05).两种肠免疫表型标志物MUC2和CDX2在早期黏膜下层浸润癌中阳性表达率均显著高于黏膜内癌,差异有统计学意义(均P<0.01).两种胃免疫表型标志物MUCSAC和MUC6在早期黏膜下层浸润癌中的阳性表达率分别为52.9%(18/34)和20.6%(7/34)均显著低于黏膜内癌91.2%(52/57)和31.6%(18/57),差异有统计学意义(P<0.01和P<0.05).在淋巴结转移阳性组和脉管浸润阳性组中,MUC2和CDX2的阳性表达率均明显高于无淋巴结转移组和无脉管浸润组,差异有统计学意义(P<0.05).随着肿瘤病变范围的扩大,CDX2阳性表达率明显增高,差异有统计学意义(P<0.05).肠型印戒细胞癌比胃型印戒细胞癌更多见于早期黏膜下层浸润癌且有更高的淋巴结转移率(P=0.000和P=0.003).生存分析显示,肠型和混合型印戒细胞癌5年生存率明显低于胃型印戒细胞癌(P<0.05).结论 肠型胃印戒细胞癌临床生物学行为和预后均较胃型印戒细胞癌差.胃、肠免疫表型标志物的胃印戒细胞癌分型有助于评估预后并有可能指导治疗.  相似文献   

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