Snail在胃癌中的表达及其临床意义

目的研究Snail在胃癌的表达与肿瘤转移的关系。方法采用免疫组化S-P法分别检测Snail在胃癌及切缘组织中的表达。结果 Snail高表达于胃癌组织的细胞核,在胃癌及切缘组织中的表达率分别为85.42%、27.08%,两者差异有统计学意义(P<0.05)。Snail高表达与胃癌分化程度、浸润深度、淋巴结转移密切相关(P<0.05)。结论胃癌中Snail高表达与肿瘤的浸润转移密切相关,Snail可能是胃癌侵袭转移的生物学标志之一。     

细胞核Snail因子在胰腺癌上皮-间质转化中的作用

目的：探讨细胞核因子Snail在胰腺癌组织中的表达及与胰腺癌上皮-间质转化（EMT）过程的相关性。 方法：采用免疫组织化学方法检测77例胰腺癌组织（研究组）与13例正常胰腺组织（对照组）中的Snail、Slug、E-cadherin、vimentin的表达。 结果：研究组中胰腺癌患者胰腺组织中Snail、Slug、E-cadherin、vimentin的表达阳性率为70.13%、68.83%、36.36%、72.73%。对照组13例正常胰腺组织中Snail、Slug均不表达,E-cadherin、vimentin的表达阳性率分别为92.31%、7.69%。胰腺癌组织中Snail表达与E-cadherin表达呈负相关（r=-0.225,P=0.025）,与vimentin表达呈正相关（r=0.493,P<0.01）;Slug表达与vimentin表达呈正相关（r=0.358,P=0.001）。Slug的表达与肿瘤分化程度及肿瘤TNM分期有关、E-cadherin的表达与淋巴结的转移与肿瘤分化程度有关、vimentin的表达与淋巴结转移、肿瘤分化程度及肿瘤TNM分期有关（均P<0.01）。 结论：Snail的高表达可能通过调控EMT过程在胰腺癌的发展过程中发挥作用,是胰腺癌浸润和转移的重要生物学指标。     

Snail介导的EMT在上皮性卵巢癌组织中的作用

目的：检测Snail、E-cadherin及Vimentin在上皮性卵巢癌组织中的表达,探讨Snail介导的上皮间质转化（EMT）在卵巢癌发生、发展及转移中的作用。方法采用免疫组化法分别检测Snail、E-cadherin、Vimentin在48例卵巢浆液性腺癌、卵巢交界性浆液性肿瘤及卵巢浆液性腺瘤中的表达,探讨EMT相关因子表达强度的相关性及与临床病理特征之间的关系。结果（1）Snail、Vimentin在卵巢浆液性腺癌中的表达率为（68.75%/66.67%）,高于卵巢交界性浆液性腺瘤的（41.67%/37.50%）及卵巢浆液性腺瘤的（25.00%/18.75%）,结果均具有显著的统计学差异（P＜0.05）,E-cadherin在卵巢浆液性腺癌中的表达率为27.08%,低于与卵巢交界性浆液性腺瘤的54.17%及卵巢浆液性腺瘤的75.00%,结果均具有统计学差异（P＜0.05）。而卵巢交界性浆液性腺瘤组与卵巢浆液性腺瘤组比较,三种蛋白的表达均无统计学差异（P＞0.05）。（2）Snail、E-cadherin及Vimentin的表达高低与FIGO分期、分化级别、有无淋巴结转移及腹膜种植有关。（3）在卵巢浆液性腺癌中,Snail与Vimentin的表达呈正相关（r=0.477,P＜0.05）,Snail与E-cadherin的表达呈负相关（r=-0.601,P＜0.05）,而E-cadherin与Vimentin表达的相关性不明显（r=-0.206, P＞0.05）。结论在上皮性卵巢癌组织中,Snail、Vimentin表达上调,E-cadherin表达下调,提示Snail介导的EMT可能与卵巢癌的发生、发展及浸润转移有关。     

转录因子Snail介导E-cadherin表达在食管鳞癌迁移和侵袭中的作用

目的探索转录因子Snail、E-cadherin基因在食管鳞癌中的表达及临床病理意义,明确其对食管鳞癌迁移和侵袭的影响。方法食管鳞癌组织及对应癌旁组织标本30例,PCR检测Snail、E-cadherin表达;以癌/癌旁组织相对表达量表示Snail及E-cadherin在mRNA水平表达的差异,分析其与临床病理特征间关系;随机抽取其中4例,Western blot检测Snail、E-cadherin表达。筛选三株食管鳞癌细胞株中的一株进行转染,利用Snail小干扰RNA作为实验组,以双链无义RNA转染作为对照组,检测Snail和E-cadherin表达水平变化,行细胞划痕、侵袭实验。结果 30例食管鳞癌组织较癌旁组织中Snail相对表达量高(1.96±0.75/0.52±0.43,P=0.04),E-cadherin相对表达量低(0.66±0.31/2.19±0.62,P=0.02);食管鳞癌中Snail相对高表达、E-cadherin相对低表达程度均与癌组织浸润深度(P=0.009)、淋巴结转移与否(P=0.047)相关。其中4例病人,癌组织相比对应癌旁组织中Snail蛋白表达高(0.73±0.13/0.23±0.08,P=0.00),而E-cadherin蛋白表达低(0.10±0.06/0.60±0.14,P=0.00)。选取EC109为实验细胞株,PCR结果显示,Snail小干扰RNA转染组较对照组中Snail表达减少(0.53±0.05/1.00±0.15,P=0.00),同时,E-cadherin表达上调(3.28±0.26/1.00±0.18,P=0.00);Western blot检测显示,抑制Snail蛋白表达后(0.25±0.05/0.41±0.10,P=0.03)EC109中E-cadherin蛋白表达上调(0.83±0.11/0.29±0.05,P=0.02)。划痕实验及Transwell细胞侵袭实验示,下调Snail表达后EC109迁移、侵袭能力均减弱(P0.05)。结论转录因子Snail在食管鳞癌中相对高表达,并可能通过介导E-cadherin表达影响肿瘤迁移与侵袭。     

上皮-间质转化及其调控基因Snail在肿瘤侵袭转移中的作用

上皮间质转化(EMT)和锌指转录因子Snail在肿瘤的侵袭和远处转移过程中起重要作用。笔者就两者在肿瘤侵袭转移中的作用结合文献进行综述。     

缺氧微环境对胰腺癌细胞发生上皮向间叶转化的诱导作用

目的 探讨胰腺癌细胞在缺氧微环境中通过发生上皮向间叶转化(EMT)从而获得侵袭性表型的可能机制.方法 在缺氧微环境下培养胰腺癌细胞Pane-1、Transwell侵袭小室对比检测细胞在缺氧微环境下侵袭能力的变化情况.Western blot、免疫荧光检测缺氧对Panc-1细胞上皮细胞标记分子E-cadherin、间叶细胞标记分子vimentin表达的影响;实时荧光定量聚合酶链反应(PCR)检测缺氧对EMT诱导因子Snail表达的影响.将编码HIF-1α cDNA的真核表达载体pCD-NA 3.1-HIF-1α瞬时转染Panc-1细胞,Western blot检测HIF-1α对E-cadherin、vimentin表达的影响.结果 常氧组细胞每高倍镜视野穿透数为(84±3)个,缺氧组为(121±5)个,差异有统计学意义(P<0.01).Panc-1细胞在常氧、缺氧12 h、缺氧24 h、缺氧48 h条件下E-cadherin蛋白的相对值分别为(0.59±0.04、54.00±0.05、0.45±0.10、0.36±0.03);vimentin蛋白的相对值分别为:(0.36±0.05、0.41±0.04、0.48±0.06、0.58±0.05),缺氧同常氧组比较差异有统计学意义(P<0.05).缺氧微环境下Panc-1细胞Snail mRNA的表达量升高,在缺氧第3天后差异具有统计学意义(P<0.05).Panc-1细胞转染HIF-1α前后,E-cadherin蛋白的相对值分别为0.63±0.05、0.47±0.07;Vvi-mentin蛋白的相对值分别为0.47±0.07、0.32±0.04,转染前后差异有统计学意义(P<0.05).结论 缺氧微环境可能通过活化HIF-lα、Snail等转录因子,促进胰腺癌细胞发生上皮向间叶转化,产生侵袭性表型.     

缺氧微环境对胰腺癌细胞发生上皮向间叶转化的诱导作用

Objective To investigate whether hypoxic environment can promote the metastasis of pancreatic cancer cells by inducing epithelial to mesenchymal transition (EMT). Methods The Panc-1 cells were cultured in hypoxia environment. After cultured for indicated periods, the in vitro invasive ability of Pane-1 cells was compared with normoxia group using Transwell invasion assay. The epithelial marker E-cadherin and the mesenchymal marker vimentin were assayed by Western blot. The expression of Snail, a strong activator of EMT, was detected by real-time PCR. The HIF-1 α encoding cDNA was transiently trans-fected into the Pane-1 cells, and the E-cadherin and vimentin were analyzed. Results The number of cells invading to the lower side of the membrane under hypoxia was ( 121±5 ), whereas only ( 84±3 ) in no-morxia group ( P < 0.05 ). The relative expression of E-cadherin in normoxia, hyoxia groups at 12,24,48 hwas (0.59±0.04 vs 54.00±0.05,0.45±0.10,0.36±0.03 ), and that of vimentin was (0.36±0.05, 0.41±0.04,0.48±0.06,0.58±0.05 ) ( P < 0.05 ). The relative expression of Snail mRNA was in-creased in hypoxia environment, and the difference was significant after 72 h ( P < 0.05 ). Before and after HIF-1α cDNA was transfected into the Panc-1 cells, the relative expression of E-cadherin was 0.63± 0.05, and 0.47±0.07, and that of vimentin was 0.47±0.07, and 0.32±0.04 respectively ( P < 0.05 ). Conclusion Hypoxia microenvironment can activate HIF-1α and Snail to trigger EMT of pancreatic cancer cells.     

缺氧微环境对胰腺癌细胞发生上皮向间叶转化的诱导作用

Objective To investigate whether hypoxic environment can promote the metastasis of pancreatic cancer cells by inducing epithelial to mesenchymal transition (EMT). Methods The Panc-1 cells were cultured in hypoxia environment. After cultured for indicated periods, the in vitro invasive ability of Pane-1 cells was compared with normoxia group using Transwell invasion assay. The epithelial marker E-cadherin and the mesenchymal marker vimentin were assayed by Western blot. The expression of Snail, a strong activator of EMT, was detected by real-time PCR. The HIF-1 α encoding cDNA was transiently trans-fected into the Pane-1 cells, and the E-cadherin and vimentin were analyzed. Results The number of cells invading to the lower side of the membrane under hypoxia was ( 121±5 ), whereas only ( 84±3 ) in no-morxia group ( P < 0.05 ). The relative expression of E-cadherin in normoxia, hyoxia groups at 12,24,48 hwas (0.59±0.04 vs 54.00±0.05,0.45±0.10,0.36±0.03 ), and that of vimentin was (0.36±0.05, 0.41±0.04,0.48±0.06,0.58±0.05 ) ( P < 0.05 ). The relative expression of Snail mRNA was in-creased in hypoxia environment, and the difference was significant after 72 h ( P < 0.05 ). Before and after HIF-1α cDNA was transfected into the Panc-1 cells, the relative expression of E-cadherin was 0.63± 0.05, and 0.47±0.07, and that of vimentin was 0.47±0.07, and 0.32±0.04 respectively ( P < 0.05 ). Conclusion Hypoxia microenvironment can activate HIF-1α and Snail to trigger EMT of pancreatic cancer cells.     

缺氧微环境对胰腺癌细胞发生上皮向间叶转化的诱导作用

Objective To investigate whether hypoxic environment can promote the metastasis of pancreatic cancer cells by inducing epithelial to mesenchymal transition (EMT). Methods The Panc-1 cells were cultured in hypoxia environment. After cultured for indicated periods, the in vitro invasive ability of Pane-1 cells was compared with normoxia group using Transwell invasion assay. The epithelial marker E-cadherin and the mesenchymal marker vimentin were assayed by Western blot. The expression of Snail, a strong activator of EMT, was detected by real-time PCR. The HIF-1 α encoding cDNA was transiently trans-fected into the Pane-1 cells, and the E-cadherin and vimentin were analyzed. Results The number of cells invading to the lower side of the membrane under hypoxia was ( 121±5 ), whereas only ( 84±3 ) in no-morxia group ( P < 0.05 ). The relative expression of E-cadherin in normoxia, hyoxia groups at 12,24,48 hwas (0.59±0.04 vs 54.00±0.05,0.45±0.10,0.36±0.03 ), and that of vimentin was (0.36±0.05, 0.41±0.04,0.48±0.06,0.58±0.05 ) ( P < 0.05 ). The relative expression of Snail mRNA was in-creased in hypoxia environment, and the difference was significant after 72 h ( P < 0.05 ). Before and after HIF-1α cDNA was transfected into the Panc-1 cells, the relative expression of E-cadherin was 0.63± 0.05, and 0.47±0.07, and that of vimentin was 0.47±0.07, and 0.32±0.04 respectively ( P < 0.05 ). Conclusion Hypoxia microenvironment can activate HIF-1α and Snail to trigger EMT of pancreatic cancer cells.     

缺氧微环境对胰腺癌细胞发生上皮向间叶转化的诱导作用

Objective To investigate whether hypoxic environment can promote the metastasis of pancreatic cancer cells by inducing epithelial to mesenchymal transition (EMT). Methods The Panc-1 cells were cultured in hypoxia environment. After cultured for indicated periods, the in vitro invasive ability of Pane-1 cells was compared with normoxia group using Transwell invasion assay. The epithelial marker E-cadherin and the mesenchymal marker vimentin were assayed by Western blot. The expression of Snail, a strong activator of EMT, was detected by real-time PCR. The HIF-1 α encoding cDNA was transiently trans-fected into the Pane-1 cells, and the E-cadherin and vimentin were analyzed. Results The number of cells invading to the lower side of the membrane under hypoxia was ( 121±5 ), whereas only ( 84±3 ) in no-morxia group ( P < 0.05 ). The relative expression of E-cadherin in normoxia, hyoxia groups at 12,24,48 hwas (0.59±0.04 vs 54.00±0.05,0.45±0.10,0.36±0.03 ), and that of vimentin was (0.36±0.05, 0.41±0.04,0.48±0.06,0.58±0.05 ) ( P < 0.05 ). The relative expression of Snail mRNA was in-creased in hypoxia environment, and the difference was significant after 72 h ( P < 0.05 ). Before and after HIF-1α cDNA was transfected into the Panc-1 cells, the relative expression of E-cadherin was 0.63± 0.05, and 0.47±0.07, and that of vimentin was 0.47±0.07, and 0.32±0.04 respectively ( P < 0.05 ). Conclusion Hypoxia microenvironment can activate HIF-1α and Snail to trigger EMT of pancreatic cancer cells.     

转录因子Snail及黏附分子E-cadherin在直肠癌中的表达及意义

目的 探讨转录因子Snail及黏附分子E-cadherin在直肠癌中的表达及意义.方法 采用免疫组化SABC法检测101例直肠癌组织中Snail、E-cadherin的表达,分析二者在不同临床病理分期与分化程度的直肠癌中的表达及其与预后的关系.结果 免疫组化检测结果显示直肠癌组织中Snail的阳性表达率为78.2%(79/101),直肠癌组织中E-cadherin的阳性表达缺失率为62.4%(63/1 01),Snail与E-cadherin的表达呈显著负相关.Snail、E-cadherin的表达与直肠癌的Dukes分期及淋巴结转移有关(P＜0.05).结论 Snail蛋白的高表达和E-cadherin蛋白的低表达可能是直肠癌侵袭转移的重要生物学标志.     

膀胱尿路上皮癌组织中Snail蛋白表达与E-cadherin蛋白、T细胞亚群的相关性分析

目的 研究膀胱尿路上皮癌组织中Snail蛋白表达与E-cadherin蛋白、T细胞亚群的相关性。 方法 采用免疫组化SP法检测156例膀胱尿路上皮癌组织和80例癌旁组织中Snail蛋白、E-cadherin蛋白的表达情况,比较二者在不同病理组织中的阳性表达率,并分析二者表达的相关性;分析膀胱尿路上皮癌组织中Snail蛋白阳性表达和CD4+、CD8+细胞数量及CD4+/CD8+的相关性。结果膀胱尿路上皮癌组织Snail蛋白阳性表达率65.4％(102/156)显著高于癌旁组织的48.8％(39/80),差异有统计学意义(P＜0.05);其表达与膀胱尿路上皮癌的临床分期、病理分级、肿瘤数量、远处转移及复发有关（P值均＜0.05）。膀胱尿路上皮癌中Snail蛋白与E-cadherin蛋白表达呈负相关（r= -0.186,P＜0.05）;Snail蛋白阳性表达与CD4+细胞数量以及CD4+/CDt+值呈负相关(r=-0.313,P＜0.05;r=-0.305,P＜0.05),而与CDs+细胞数量无关（r= -0.250,P＞0.05）。 结论 Snail蛋白可能通过抑制E-cadherin蛋白表达及诱导膀胱肿瘤局部免疫抑制,促进膀胱尿路上皮癌的浸润、转移。     

原发性肝细胞癌中错配修复基因hMLH1的表达及其意义

目的　探讨错配修复基因hMLH1在原发性肝细胞癌(HCC)组织中的表达及其意义。方法　采用免疫组织化学和逆转录 聚合酶链反应(RT PCR)检测48例肝癌组织、2 3例癌旁组织和2 5例正常肝组织中hMLH1蛋白和mRNA的表达情况,同时采用原位末端标记法测定癌组织的细胞凋亡指数。结果　48例肝癌组织、2 3例癌旁组织和2 5例正常肝组织的hMLH1mRNA表达分别为62 .5 % (3 0 /4 8)、10 0 .0 % (2 3 /2 3 )和10 0 .0 % (2 5 /2 5 ) ,蛋白表达分别为60 .41% (2 9/4 8)、91.3 0 % (2 1/2 3 )和10 0 .0 0 % (2 5 /2 5 )。hMLH 1表达与肝癌组织的临床分期有明显相关,hMLH1表达阳性的肝癌组织的细胞凋亡指数升高为(3 .5 62±0 .2 3 3 ) %。结论　hMLH1在肝癌组织中低表达,提示错配修复基因hMLH1功能缺陷在肝癌的发生、发展过程中起重要作用     

GPC3 mRNA在甲胎蛋白阴性肝癌中的表达及其意义

目的 探讨GPC3基因在甲胎蛋白阴性肝癌中的变化及其临床意义。方法 应用印迹法（Northern)杂交检测48例肝癌组织及其相应的癌旁肝细胞内GPC3mRNA表达的变化,其中肝细胞癌41例、肝内胆管细胞癌4例、大肠癌肝转移2例和肝局灶性结节增生1例,并结合各组织标本的病理学特点进行分析。结果 41例甲胎蛋白阴性肝细胞癌中,有30例肝癌组织可测出GPC3mRNA的表达（73.17%),而癌旁组织中均不表达。直径＞5cm的大肝癌GPC3的表达率显著高于直径≤5cm的小肝癌,低分化肝癌GPC3 的表达率显著高于高分化的肝癌。GPC3的表达与患者的年龄、性别、包膜完整性、癌栓形成、肝内转移及乙肝病毒感染状况均无明显相关性。GPC3mRNA在非肝细胞肝癌组织内均不表达。结论 GPC3mRNA在AFP阴性肝癌中特异性表达,可作为原发性肝癌的一个新的基因标志。GPC3mRNA在肝癌的发生发展中有重要作用。     

肝细胞癌中SEMA3B基因的表达及其意义

目的 通过对SEMA3B基因在原发性肝细胞癌（HCC）组织中表达的检测，探讨该基因与HCC发生机制的关系。方法 采用逆转录-聚合酶链反应（RT—PCR）方法检测35例HCC组织及癌旁肝组织SEMA3BmRNA表达水平。结果 （1）在所有受检的癌旁肝组织中，SEMA3BmRNA表达率为85．7％（30／35），明显高于癌组织的表达率20．0％（7／35），差异有统计学意义（P〈0．01）；（2）合并有肝硬化（20／28）或者乙肝（19／28）的患者，其癌组织中SEMA3B基因的表达缺失率显著高于无肝硬化（8／28）或乙肝阴性（9／28）患者（P〈0．05）；（3）SEMA3B基因的异常表达情况与年龄、性别的差异无统计学意义（P〉0．05），与HCC患者术前肝功能Child—Pugh分级评价和血清AFP的检测值高低无相关（P〉0．05）；（4）SEMA3B的表达缺失率与TNM分期关系无统计学差异，低分化型癌组织中SEMA3B基因缺失率高于中、高分化型，但差异无统计学意义（P〉0．05）。此外，该基因的缺失与肿瘤大小无关（P〉0．05）。结论 SEMA3B基因在HCC组织中的高频表达缺失说明该基因的失活与HCC的发生密切相关。SEMA3B基因是定位于染色体3p21．3区域的与HCC相关的抑癌基因，并且可能在HCC的发生发展方面起重要作用。     

大肠癌中Cyclin E表达及其意义

目的：研究大肠癌中Cyclin E表达及其意义。方法：采用流式细胞术（FCM)对30例大肠癌实体瘤的癌组织和远切端正常组织Cyclin E表达率及细胞增殖指标（PI，SPF）进行检测，将Cyclin E阳性表达率与大肠癌临床病理指标进行比较，PI，SPF进行相关性分析。结果：大肠癌肿瘤组织的Cyclin E的阳性表达率及PI，SPF明显高于远癌切端正常组织，与肿瘤的恶性程度，淋巴结转移及发生部位无显著相关，与肿瘤细胞的增殖活性相关，在增生活跃的肿瘤细胞中Cyclin E伯表达率高。结论；Cyclin E过表达参与了大肠癌的发生，Cyclin E表达率与传统的临床病理指标无关，但与细胞增殖活性有明显相关性。Cyclin E表达率可能成为另一个判断大肠癌预后的指标。     

原发性肝癌多药耐药基因的表达及意义

目的 探讨５种多药耐药（ＭＤＲ）基因在肝癌组织中的表达,建立ＭＤＲ的基因诊断标准。方法 用逆转录ＰＣＲ、流式细胞术检测肝癌组织中５种ＭＤＲ基因ｍＲＮＡ和蛋白质的表达,用ＭＴＴ法检测抗癌药物对肝癌原代细胞的ＩＣ５０值。结果 肝癌耐药涉及ｍｄｒ１、ＭＲＰ、ＬＲＰ、ＧＳＴＰ１和ＴｏｐｏⅡα基因。ｍｄｒ１ ｍＲＮＡ≥０．５、ＭＲＰ ｍＲＮＡ≥０．６、ＬＲＰ ｍＲＮＡ≥０．８、ＧＳＴＰ１ ｍＲＮＡ≥０．７Ｔ ＴｏｐｏⅡαｍＲＮＡ≤０．４为耐药联合诊断标准,符合率为９８．００％。结论 多重ＭＤＲ是肝癌耐药的主要形式。用逆转录ＰＣＲ方法联合检测５种ＭＤＲ基因ｍＲＮＡ表达在肝癌化疗敏感性预测中具有必要性和可行性。     

Ku80基因在人原发性肝癌组织中的表达及其生物学意义

目的 探讨Ku80基因在人原发性肝癌的表达及其表达水平与肝癌的生物学特征的关系.方法 采用免疫组织、细胞化学技术及Westem blot技术,检测40例在同济医院肝脏外科中心行手术切除的原发性肝细胞癌患者的肝癌组织及癌旁组织、肝癌细胞系HepG2细胞及正常肝细胞系L02细胞中Ku80的表达,分析Ku80表达水平与肝癌、肝癌的分化程度及转移特性的关系.结果 Ku80在肝癌组织中的表达明显低于在癌旁肝组织中的表达,分别为14.95%和43.78%,差异有统计学意义(P<0.01);Ku80在低分化肝和中、高分化肝癌组织中的表达率分别为16.05%和13.85%,差异无统计学意义(P>0.05);伴有门静脉癌栓和不伴有门静脉癌栓的肝癌组织中Ku80的表达率分别为14.81%和16.31%,差异无统计学意义(P>0.05).结论 Ku80基因在人原发性肝细胞癌组织中表达显著下调,表明Ku80表达下调与原发性肝细胞癌的发生密切相关,但与肝癌的分化程度、转移特征无明显相关.     

RASSF1A在胰腺癌组织中的表达及其临床意义

目的 探讨押癌基因RASSF1A在胰腺癌组织中的表达及其与胰腺癌发生、发展的关系.方法 采用逆转录-聚合酶链反应(RT-PCR)方法检测48例胰腺癌组织及癌旁正常组织RASSFA mRNA的表达水平.结果 癌旁正常组织RASSF1A mRNA的表达量高于高分化腺癌组织RASSF1A的表达量,差异有统计学意义(P<0.05).高分化腺癌组织RASSF1A mRNA的表达量高于中低分化腺癌组织,差异有统计学意义(P<0.01).TNM分期Ⅲ期RASSF1A mRNA的表达量低于Ⅰ、Ⅱ期,差异有统计学意义(P<0.05).RASSF1A mRNA表达与性别、年龄,肿瘤发生部位无明显关系(P>0.05).结论 RASSF1A表达缺失或低下在胰腺癌的发生、发展中起重要的作用.