胰腺癌组织中p53、血管内皮生长因子的表达与血管生成的关系及其临床意义

目的探讨胰腺癌组织中p53、血管内皮生长因子(VEGF)和血管生成的关系.方法用免疫组织化学方法检测48例胰腺癌组织及癌旁组织、6例正常胰腺组织中p53、VEGF表达和微血管密度(MVD).结果胰腺癌组织中VEGF、p53的阳性表达率分别为54.17%和50%,显著高于癌旁组织及正常组织的表达率(P < 0.01),胰腺癌组织中MVD显著高于癌旁组织及正常组织.VEGF表达与肿瘤大小和分期有关(P=0.038,P=0.045),VEGF表达与MVD有相关性(r=0.294 P=0.043).p53与淋巴结转移及预后相关(P < 0.05)而与VEGF、MVD之间无关.MVD与胰腺癌临床病理特征无关,MVD与生存期存在负相关(r=-0.371 P=0.011).多元回归分析显示p53、VEGF和MVD都不是影响胰腺癌预后的独立因素.结论 p53基因突变为胰腺癌分子事件的晚期事件,可作为评价胰腺癌预后的一项指标,抗血管生成可能有利于胰腺癌的治疗.     

胰腺癌组织中p53、血管内皮生长因子的表达与血管生成的关系及其临床意义

目的 探讨胰腺癌组织中p53、血管内皮生长因子(VEGF)和血管生成的关系。方法 用免疫组织化学方法检测48例胰腺癌组织及癌旁组织、6例正常胰腺组织中p53、VEGF表达和微血管密度(MVD)。结果 胰腺癌组织中VEGF、p53的阳性表达率分别为54.17％和50％,显著高于癌旁组织及正常组织的表达率(P<0.01),胰腺癌组织中MVD显著高于癌旁组织及正常组织。VEGF表达与肿瘤大小和分期有关(P=0.038,P=0.045),VEGF表达与MVD有相关性(r=0.294 P=0.043)。p53与淋巴结转移及预后相关(P<0.05)而与VEGF、MVD之间无关。MVD与胰腺癌临床病理特征无关,MVD与生存期存在负相关(r=0.371 P=0.011)。多元回归分析显示p53、VEGF和MVD都不是影响胰腺癌预后的独立因素。结论 p53基因突变为胰腺癌分子事件的晚期事件,可作为评价胰腺癌预后的一项指标,抗血管生成可能有利于胰腺癌的治疗。     

非肌层浸润性膀胱癌组织Ki-67、p53和CK-20表达变化及其临床意义

目的 探讨非肌层浸润性膀胱癌（NMIBC）组织Ki-67、p53、细胞角蛋白20(CK-20)表达变化及其临床意义。方法 选择NMIBC患者105例，取手术切除的NMIBC组织及其配对的癌旁正常组织，采用免疫组化法检测Ki-67、p53、CK-20表达。比较NMIBC组织与癌旁正常组织Ki-67、p53、CK-20阳性表达，分析NMIBC组织Ki-67、p53、CK-20表达与患者临床病理特征的关系以及三者表达的关系。结果 NMIBC组织Ki-67、p53、CK-20阳性表达率均显著高于癌旁正常组织（χ2分别为40.485、40.752、42.091,P均<0.01）。NMIBC组织Ki-67、p53、CK-20表达与病理分级、浸润深度、术后复发有关（P均<0.05），而与性别、年龄、肿瘤数目、肿瘤最大径无关（P均>0.05）。NMIBC组织Ki-67阳性表达与p53、CK-20阳性表达均呈正相关关系（r分别为0.642、0.669,P均<0.01）,p53阳性表达与CK-20阳性表达亦呈正相关关系（r=0.706,P<0.01）。结论 NMIBC组织Ki...     

Ki-67和p53在壶腹癌中的表达及预后意义

目的研究壶腹癌中Ki-67和p53的表达及预后意义,探讨两者在壶腹癌发生和发展中的作用。方法应用全自动免疫组化方法分别检测Ki-67和p53在40例行胰十二指肠切除术(pancreaticoduodenectomy,PD)后壶腹癌患者中的表达,分析两者与患者临床病理资料的关系及预后。结果 40例患者纳入研究,患者1、3、5年累积生存率分别为98%、67%和44%。40例壶腹癌组织中Ki-67阳性率92.5%(37/40),p53阳性率67.5%(27/40)。Ki-67在不同浸润程度的壶腹癌中表达差异有统计学意义(P=0.011)。单因素生存分析表明,Ki-67(P=0.006)和p53(P=0.021)的表达及肿瘤的浸润程度(P=0.024)与壶腹癌患者的生存时间相关,而肿瘤最大直径、分化程度、淋巴结转移、TNM分期、血清CA19-9等因素与壶腹癌预后无明显相关性;多因素生存分析显示,p53是影响壶腹癌患者长期生存的独立因素(OR=1.717,P=0.015)。结论 Ki-67在壶腹癌的发生和发展中起重要作用,其表达有助于阐释壶腹癌浸润生长的机制;p53过表达可作为评估壶腹癌预后的参考指标。     

结直肠癌组织中Ki-67和pAKT的表达及其临床意义

[目的]探讨结直肠癌组织中Ki-67和pAKT的表达及其临床意义,为临床诊治结直肠癌提供依据。[方法]选取结直肠癌患者80例,患者均经病理确诊为结直肠癌。应用免疫组织化学SP法检测80例结直肠癌组织(结直肠癌组)、80例结直肠癌癌旁组织(癌旁组)、20例正常大肠组织(正常组)中Ki-67和pAKT的表达阳性率。分析结直肠癌患者癌组织中Ki-67和pAKT表达与结直肠癌转移、分期及预后的关系。采用Spearman相关分析法分析Ki-67及pAKT表达的相关性。[结果]结直肠癌组中Ki-67和pAKT的表达阳性率明显高于癌旁组和正常组的阳性率(P=0.000,0.000,0.012)(P=0.000,0.011,0.024)。有淋巴结转移的患者癌变组织中Ki-67和pAKT表达阳性率明显高于无淋巴结转移患者(P=0.013,P=0.009);Ⅰ+Ⅱ期患者癌组织中Ki-67和pAKT表达阳性率明显低于Ⅲ+Ⅳ分期(P=0.003,P=0.002);Ki-67与pAKT表达呈正相关关系(r=0.520,P=0.020);Ki-67阴性表达患者总生存率与Ki-67表达(+)、(++)及(+++)的患者总生存率比较差异有统计学意义(P=0.021,0.022,0.000);pAKT阴性表达患者总生存率与pAKT表达(+)、(++)及(+++)的患者总生存率比较差异有统计学意义(P=0.011,0.012,0.001)。[结论]Ki-67和pAKT异常表达与结直肠癌的发生发展密切相关,其表达上调参与肿瘤形成、发展、侵袭和转移,可作为判断结肠癌生物学行为的临床参考指标。     

肝细胞癌中金属硫蛋白表达下调及其临床病理学意义

目的:研究MT在肝细胞癌(HCC)中的表达和定位及其与临床病理特征.方法:对400例外科切除的HCC及相应非癌肝组织标本构建组织芯片,用EnVision Plus法进行MT,P53和Ki-67免疫组织化学染色.结果:与相应的非癌肝组织相比,HCC组织MT的表达显著下调,HBsAg阳性患者MT阳性率显著低于阴性者(P=0.042),肿瘤直径≤2 cm的MT阳性率显著高于肿瘤直径＞2 cm者(P=0.007).随着组织学分级进程,MT表达呈降低趋势(P=0.004),MT核内表达与低分化HCC密切相关.MT与P53及Ki-67的表达无统计学相关性.结论:HCC中MT表达下调在肝癌的发生过程中有一定作用,可能是肝细胞分化的一个标志物,HBsAg与MT表达下调有关,以核染色为主的MT表达可能反映了低分化HCC的一种侵袭性行为.     

胰腺癌组织中SATB1和Ki-67的表达变化及意义

目的 观察核基质结合区结合蛋白1（SATB1）和Ki-67在胰腺癌组织中的表达变化,并探讨其意义.方法 应用免疫组化SP法检测58例胰腺癌组织、配对癌旁组织及正常胰腺组织中SATB1和Ki-67的表达,将二者在胰腺癌中的表达水平与临床病理参数的关系进行统计学分析.结果 SATB1和Ki-67在胰腺癌中的阳性表达率分别为63.8％ （37/58）、70.7％ （41/58）,且在胰腺癌、癌旁组织及正常组织中的表达呈下降趋势.胰腺癌组织中SATB1的表达与患者年龄、T分期、淋巴结转移和TNM分期相关（P＜0.05）,Ki-67的表达与T分期、淋巴结转移和TNM分期相关（P＜0.05）.Cox分析显示,SATB1（RR=18.625,95％ CI为11.178 ～ 285.631）和Ki-67（RR=1.985,95％ CI为0.394～ 320.525）是影响胰腺癌患者预后的独立因素（P均＜0.05）.结论 SATB1和Ki-67在胰腺癌组织中高表达,可作为胰腺癌发生发展的预测指标之一.     

EGFR、P53、Ki-67在结直肠癌中表达及临床病理学意义

目的研究表皮生长因子受体(EGFR)、P53、Ki-67在结直肠癌中的表达及其与临床病理特征之间的关系。方法应用S-P免疫组化方法,检测结直肠癌中EGFR、P53、Ki-67的表达情况;并分析其与临床病理特征的相关性。结果 87例结直肠癌患者中,EGFR、P53和Ki-67的阳性率分别为35.6%(31/87)、65.5%(57/87)和95.4%(83/87);EGFR、P53和Ki-67的表达水平与患者性别、年龄及大体类型无相关性(P0.05);Ki-67、P53、EGFR在结直肠癌不同分化程度、TNM分期及淋巴结转移组间表达差异有统计学意义(P0.05);且三者在结直肠癌组织中的表达明显高于癌旁正常肠黏膜(P0.05)。EGFR与p53表达呈正相关性(P0.05);Ki-67与P53、EGFR无相关性(P0.05)。结论联合检测EGFR、P53和Ki-67在结直肠癌中的表达有利于对肿瘤恶性程度及患者预后进行评估,并为临床治疗提供分子生物学支持。     

胰腺癌组织中VEGF、PCNA与血管生成的关系及预后相关性

目的探讨胰腺癌组织中VEGF、PCNA和血管生成的关系.方法用免疫组织化学方法检测48例胰腺癌及癌旁组织、6例正常胰腺组织中VEGF、PCNA的表达和微血管密度(MVD).结果胰腺癌组织中VEGF、PCNA的阳性表达率分别为54.17%和77.5%,显著高于癌旁组织和正常组织的表达率(P < 0.01),胰腺癌组织中MVD显著高于癌旁组织和正常组织.VEGF表达与肿瘤大小和TNM分期有关(P = 0.020, P = 0.045),并且与MVD有相关性(r = 0.294, P = 0.043).PCNA与临床病理因素无关.多元回归分析显示VEGF、PCNA和MVD都不是影响胰腺癌预后的独立因素.结论血管生成在胰腺癌的发生、发展过程中起重要作用,抗肿瘤血管生成可能会提高胰腺癌的治疗效果.     

胃癌组织FAT10与突变型p53表达及其相互关系

目的 检测FAT10与突变型p53在胃癌组织中的表达情况及相互间关系.方法 采用免疫组化和逆转录-聚合酶链反应(RT-PCR)方法检测FAT10和突变型p53在62例胃癌患者的胃癌组织、癌旁组织(距癌边缘2～5 cm)及正常胃组织(距癌边缘>5 cm)中的表达水平,统计分析两者表达间的关联性及FAT10与胃癌预后之间的关系.结果 FAT10蛋白和突变型p53蛋白在胃癌组织中的表达阳性率分别为51.61%(32/62)和45.16%(28/62),显著高于癌旁组织[12.90%(8/62)和14.51%(9/62),χ2值分别=21.26和20.69,P值均<0.01]及正常胃组织[6.45%(4/62)和9.68%(6/62),χ2值分别=13.91和19.61,P值均<0.01].胃癌FAT10蛋白及mRNA的表达上升主要与胃癌的淋巴转移及TNM分期密切相关(P值均<0.05).胃癌组织中FAT10表达在蛋白及基因水平均与突变型p53表达呈正相关性(r值分别=0.865和0.761,P值分别<0.05和0.01).FAT10蛋白阳性表达或mRNA表达水平高者,其累计生存时间显著低于FAT10阴性者(P值均<0.05).结论 FAT10与突变型p53在胃癌组织中表达上调且呈正相关性,两者可能共同参与胃癌的形成与发展,FAT10对评价胃癌的预后可能有较好的价值.     

Ki-67、VEGF、Cyclin D1的表达与肝细胞癌生物学行为的关系

目的:探讨肝细胞癌(hepatocellular carcinoma,HCC)、胆管癌、肝硬化及正常肝组织中增殖细胞核抗原(Ki-67)、血管内皮生长因子(vascular endothelial growth factor,VEGF)及周期素D1(Cyclin D1)蛋白表达的意义及其与肝癌生物学行为关系.方法:对HCC组织52例、胆管癌组织10例、肝硬化组织10例及正常肝组织10例,采用免疫组织化学S-P法检测Ki-67、VEGF及Cyclin D1蛋白.结果:Ki-67、VEGF及Cyclin D1在HCC的强阳性表达率分别为48.1%、55.8%及55.8%,均显著高于胆管癌、肝硬化及正常肝组织(?2=15.672、15.524、14.812,P<0.001).Ki-67与肿瘤大小、血管侵犯、分化程度有关;VEGF、Cyclin D1表达与肿瘤包膜完整、血管侵犯及肿瘤分化程度明显有关;Ki-67与VEGF及Cyclin D1间无相关.VEGF与Cyclin D1间的蛋白表达呈正相关(r=0.374,P<0.01).结论:Ki-67、VEGF及Cyclin D1表达与肝细胞癌生物学行为密切相关,与肝癌的发生和发展密切相关.关键词:肝细胞癌;增殖细胞核抗原;血管内皮生长因子;周期素D1;免疫组织化学     

Prognostic role of p53 and Ki-67 immunohistochemical expression in patients with surgically resected lung adenocarcinoma: a retrospective study

Objective

p53 mutations and the Ki-67 protein are frequently observed in various types of human cancer; the abnormal expression of p53 and Ki-67 in the tumor is associated with poor survival of lung cancer patients. We aimed to assess the prognostic role of immunohistochemical (IHC) expression of p53 and Ki-67 in lung adenocarcinoma tissue.

Methods

Tumor samples from 136 patients who had undergone surgical resection for lung adenocarcinoma were retrospectively evaluated for p53 and Ki-67 expression by immunohistochemistry. Associations of clinical and pathologic variables with p53 and Ki-67 were determined using the χ² test. After excluding two patients (follow-up loss), 134 cases were evaluated for associations between p53, Ki-67, clinical and pathologic variables, and survival by using the Cox proportional hazards regression model and Kaplan-Meier method.

Results

In the 136 patients, p53 was positive in 71.0% (93/131), and Ki-67 showed high in 49.2% (61/124). Unlike p53, Ki-67 was associated with male sex, smoking, and poor tumor differentiation (P=0.004, P=0.001 and P=0.006). Of these, poor tumor differentiation strongly was correlated with high level of Ki-67 expression (P=0.008). Neither p53 nor Ki-67 was associated with increased risk of death (P=0.318, P=0.053); however, age ≥60 years and lymph node involvement were significant predictors of death (P=0.039 and P=0.042). The log-rank test revealed a significant association between Ki-67 and lower survival in all patients (χ²=5637; P=0.018); however, the risk was limited to stage III cases (χ²=5.939; P=0.015). Unlike p53, patients with high level of Ki-67 expression showed lower 3-year actuarial survival than those without (log-rank test, χ²=4.936; P=0.026).

Conclusions

IHC expression of Ki-67 in lung adenocarcinoma tissue shows stronger association with poor tumor differentiation, and negatively affects patients’ survival in advanced-stage lung cancer; however, the role of p53 on patient outcome needs further study.     

Mutated p53 protein expression and proliferative activity in advanced gastric cancer.

BACKGROUND/AIMS: When the DNA of cells is damaged, wild-type p53 protein induces the expression of p21 (Waf1/Cip1/Sdi1), and regulates the progression of the cell cycle by inducing G1 arrest. Thus, wild type p53 or p21 protein negatively regulates cancer cell proliferation. However, in tumor with loss of expression of functional wild-type p53 protein by mutation or allelic deletion of the gene for p53, whether the proliferative activity of cancer cells might be accelerated or not is unclear. In this study, we investigated the correlation between the level of expression of mutated p53 protein and the proliferative activity of cancer cells in advanced gastric cancer. METHODOLOGY: Ninety-seven samples from patients with gastric cancer that had invaded the serosa without lymph node metastasis (t3, n0, stage II) were investigated by immunohistochemical staining with a monoclonal antibody against p53 and against p21, and with the monoclonal antibody Ki-67. DNA ploidy patterns were analyzed by flow cytometry. The immunoreactivity against p53 and the proliferative activity of cancer cells were scored in terms of a labeling index (LI; percentage of immunostained cells) in each case. Moreover, the prognostic values for 93 surviving patients were evaluated by univariate and multivariate analysis. RESULTS: The mean p53 LI was 24% (range: 0-82.4%) and the mean Ki-67 LI was 23.1% (range: 0-70.7%) in 97 tumors. The expression of p21 protein was detected in 30 of 97 tumors (30.9%) and DNA aneuploidy was detected in 36 of 97 tumors (37.1%). There was significant correlation between the p53 LI and the Ki-67 LI (r = 0.61, t = 7.456, p < 0.001) in 97 tumors. Although, no significant difference was detected, the mean p53 LI (18.3%) of 30 tumors with expression of p21 protein was lower than that of 67 tumors without expression of p21 protein (26.6%, p = 0.096). However, no significant correlation between expression of p21 protein and Ki-67 LI was observed. The p53 LI was not an independent prognostic factor in 93 surviving patients by multivariate survival analysis (p = 0.069). However, the 5-year survival rate of 50 patients with a low level of p53 LI (p53 LI (< or = 10%, 78.3%) was significantly better than that of 43 patients with a high level of p53 LI (p53 LI > 10%, 62.1%, p = 0.045). CONCLUSIONS: Accumulation of mutated p53 protein might suppress the expression of p21 protein in gastric adenocarcinoma, and cancer cells with overexpression of mutated p53 protein might have a high proliferative activity.     

Insulin receptor substrate 1 may play divergent roles in human colorectal cancer development and progression

BACKGROUND Despite effective prevention and screening methods, the incidence and mortality rates associated with colorectal cancer(CRC) are still high. Insulin receptor substrate 1(IRS-1), a signaling molecule involved in cell proliferation, survival and metabolic responses has been implicated in carcinogenic processes in various cellular and animal models. However, the role of IRS-1 in CRC biology and its value as a clinical CRC biomarker has not been well defined.AIM To evaluate if and how IRS-1 expression and its associations with the apoptotic and proliferation tumor markers, Bax, Bcl-x L and Ki-67 are related to clinicopathological features in human CRC.METHODS The expression of IRS-1, Bax, Bcl-x L and Ki-67 proteins was assessed in tissue samples obtained from 127 patients with primary CRC using immunohistochemical methods. The assays were performed using specific antibodies against IRS-1, Bax, Bcl-x L, Ki-67. The associations between the expression of IRS-1, Bax, Bcl-x L, Ki-67 were analyzed in relation to clinicopathological parameters, i.e., patient age, sex, primary localization of tumor, histopathological type, grading, staging and lymph node spread. Correlationsbetween variables were examined by Spearman rank correlation test and Fisher exact test with a level of significance at P 0.05.RESULTS Immunohistochemical analysis of 127 CRC tissue samples revealed weak cytoplasmatic staining for IRS-1 in 66 CRC sections and strong cytoplasmatic staining in 61 cases. IRS-1 expression at any level in primary CRC was associated with tumor grade(69% in moderately differentiated tumors, G2 vs 31% in poorly differentiated tumors, G3) and with histological type(81.9% in adenocarcinoma vs 18.1% in adenocarcinoma with mucosal component cases). Strong IRS-1 positivity was observed more frequently in adenocarcinoma cases(95.1%) and in moderately differentiated tumors(85.2%). We also found statistically significant correlations between expression of IRS-1 and both Bax and Bcl-x L in all CRC cases examined. The relationships between studied proteins were related to clinicopathological parameters of CRC. No significant correlation between the expression of IRS-1 and proliferation marker Ki-67, excluding early stage tumors, where the correlation was positive and on a high level(P = 0.043, r = 0.723).CONCLUSION This study suggests that IRS-1 is co-expressed with both pro-and antiapoptotic markers and all these proteins are more prevalent in more differentiated CRC than in poorly differentiated CRC.     

PDK1在胰腺癌中的表达及其临床意义

目的:探讨PDK1在胰腺癌中的表达及其与临床病理特征的关系.方法:对44例胰腺癌及其癌旁正常组织标本,分别应用RT-PCR方法和Western blot方法检测其PDK1的mRNA和蛋白表达,并和临床病理指标进行统计学分析.结果:经RT-PCR检测胰腺癌组织中PDK1表达水平明显高于癌旁正常组织(0.352006 vs 0.074887,P<0.01);Western blot检测发现72.727%(32/44)PDK1蛋白的表达癌组织中高于癌旁组织,有统计学差异(P<0.01).PDK1在胰腺癌组织中的表达与患者性别、年龄、肿瘤大小和分化程度均无相关性(P>0.05),而与T分期、淋巴结转移和TNM分期密切相关(P<0.05).结论:PDK1在胰腺癌中表达上调,可能与胰腺癌发生、发展及转移有关.     

Expression of Ki-67, p53, and K-ras in chronic pancreatitis and pancreatic ductal adenocarcinoma

AIM: To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic cancer. METHODS: We examined expression of Ki-67, CEA, p53, and K-ras, in the surgical specimens of pancreas with adenocarcinomas (n= 11) and chronic pancreatitis (n = 12). Cellular proliferation was assessed by Ki-67 proliferation index using the proliferation marker Ki-67. In specimens with pancreas cancer, we divided pancreas epithelium into normal (n = 7), ductal hyperplasia (n = 3), dysplasia (n = 4), and cancerous lesion (n = 11) after hematoxylin and eosin staining, Ki-67, and CEA immunohistochemical staining. In cases with chronic pancreatitis, the specimen was pathologically examined as in cases with pancreas cancer, and they were also determined as normal (n = 10), ductal hyperplasia (n = 4), or dysplasia (n = 5). p53 and K-ras expression were also studied by immunohistochemical staining. RESULTS: In pancreatic cancer, the Ki-67 index was 3.73±3.58 in normal site, 6.62±4.39 in ductal hyperplasia, 13.47±4.02 in dysplasia and 37.03±10.05 in cancer tissue, respectively. Overall, p53 was positive in normal ducts, ductal hyperplasia, dysplasia, and carcinoma cells in 0 of 14 (0%), 0 of 7(0%), 7 of 9 (78%), and 10 of 11 (91%), respectively, and K-ras was positive in 0 of 8 (0%), 1 of 3 (33%), 4 of 6 (67%), 4 of 5 (80%), respectively. CONCLUSION: Our results favorably support the hypothesis that ductal hyperplasia and dysplasia of the pancreas might be precursor lesions for pancreas cancer. Further evaluation of oncogenes by the molecular study is needed.     

Ezrin和HER2在胃癌组织芯片中的表达及意义

目的:探讨Ezrin蛋白在胃癌组织中的表达,与肿瘤浸润、转移的关系及与HER2的相互作用.方法:485例原发性胃癌组织中高、中、低分化胃癌分别为19例、235例和231例;有淋巴结转移者353例;TNM分期Ⅰ、Ⅱ期166例,Ⅲ、Ⅳ期319例.另外取距肿瘤7cm的正常胃黏膜组织40例.制成8个组织芯片蜡块,用免疫组织化学方法检测石蜡包埋的胃及胃癌组织中的Ezrin和人类表皮生长因子受体2(hum an epidermal growth factor receptor 2,HER2)蛋白表达.所有患者均经外科手术治疗,病理诊断明确,术前未经放、化疗.结果:Ezrin和HER2在胃癌组织中高表达,二者均与肿瘤Lauren’s分型和肿瘤分化程度相关(χ2=17.625,χ2=20.386,均P=0.000;χ2=9.474,P=0.009,χ2=13.377,P=0.010);Ezrin同时还与组织学(日本分型)、TNM分期、浸润深度和淋巴结转移相关(χ2=37.542,P=0.000;χ2=12.237,P=0.002;χ2=21.194,P=0.002;χ2=9.868,P=0.007).Ezrin和HER2蛋白表达呈正相关(r=0.129,P=0.004).结论:Ezrin可能是预测胃癌组织浸润、转移有用的指标;联合检测Ezrin和HER2可作为判断胃癌预后、筛选高危转移患者的有效指标并有可能用于指导胃癌的个体化治疗.     

ANXA2和ANXA4在胃腺癌中的表达及临床意义

目的:研究膜联蛋白A2(AnnexinA2,ANXA2)、膜联蛋白A4(AnnexinA4,ANXA4)在人体胃腺癌(gastric adenocarcinoma cells,GAC)的表达,探讨其表达与GAC生物学行为的关系及两种蛋白的相关性.方法:免疫组织化学SP法检测组织芯片中75对配对的GAC和其相应癌旁组织ANXA2和ANXA4的表达.结果:在GAC和癌旁组织中ANXA2、ANXA4的表达分别为:33.1%(25)vs1.3%(1)、68.0%(51)vs25.5%(13),二者在GAC的表达显著高于癌旁组织(x2=24.448,P=0.000;x2=39.353,P=0.000);ANXA2和ANXA4在GAC表达呈正相关(r=0.335,P=0.003);两种蛋白的表达与GAC的浸润深度、淋巴结转移、TNM分期和分化程度有关(P<0.05),与年龄、性别和远处转移无关(P>0.05);肿瘤大小与ANXA2表达有关(P<0.01),与ANXA4表达无关(P>0.05).结论:ANXA2和ANXA4的表达上调可能共同参与了GAC的发生、发展、浸润和转移,可作为临床预测GAC预后的标志物和治疗靶点.