载脂蛋白E和补体C4b1在人胰腺癌组织中的表达及意义

目的 检测载脂蛋白E(ApoE)和补体C4b1在人胰腺癌组织中的表达,探讨其意义.方法 应用免疫组化法检测38例胰腺癌和相应癌旁正常胰腺组织ApoE、C4b1蛋白表达;应用RT-PCR法检测20例胰腺癌和相应癌旁正常胰腺组织ApoE、C4b1 mRNA表达.分析ApoE、C4b1的表达与胰腺癌生物特征的相关性.结果 胰腺癌组织ApoE、C4b1蛋白表达阳性率分别为86.8%(33/38)和76.3%(29/38),显著高于癌旁正常胰腺组织的42.1%(16/38)和26.3%(10/38)(P值均＜0.01);有淋巴结转移的胰腺癌组织ApoE、C4b1蛋白表达阳性率分别为78.3%(18/23)和73.9%(17/23),明显高于无转移者的33.3%(5/15)和40.0%(6/15)(P值均＜0.05).胰腺癌ApoE、C4b1 mRNA表达量分别为4.83±0.65、7.94±0.95,明显高于癌旁正常胰腺组织的1.78±0.74、1.22±0.57(P值均＜0.01);有淋巴结转移的胰腺癌组织ApoE、C4b1 mRNA的表达量为5.05±0.71、8.24±1.07,显著高于无转移者的4.42±0.25、7.39±0.15(P值均＜0.05).结论 ApoE、C4b1在胰腺癌组织中高表达,并与胰腺癌淋巴结转移相关.     

Expression of Ezrin, HGF, C-met in pancreatic cancer and non-cancerous pancreatic tissues of rats

BACKGROUND:Recent studies have confirmed that the expression of Ezrin,hepatocyte growth factor(HGF)and its receptor(C-met)is related to the genesis,progress,invasion and metastasis of some malignant tumors.Researches have also found that the biological function of Ezrin is closely related to HGF/C-met in malignant tumors.However,there is no report on the expression levels of Ezrin,HGF and C-met in rat pancreatic cancer induced by dimethylbenzanthracene (DMBA).This study aimed to detect the expression of Ezrin, HGF and C-met in rat pancreatic cancer and non-cancerous pancreatic tissues,and assess its effect in cancer induction by DMBA. METHODS:Ninety Sprague-Dawley rats were divided into 3 groups randomly:40 in a pancreatic cancer model group (group A),40 in a trichostatin A(TSA)intervention group (group B),and 10 in a control group(group C).DMBA was directly implanted into the parenchyma of rat pancreas in group A+group B.The rats of group B were treated with 1 ml of TSA saline solution(1μg/ml)via intraperitoneal injection weekly.The carcinogenesis of rats executed within 3-5 months in groups A and B was observed by macrograph and microscopy. Meanwhile,the rats in group C were executed within 5 months. The EnVision TM immunohistochemistry for detecting the expression levels of Ezrin,HGF and C-met was used in paraffinembedded sections of the pancreatic specimens. RESULTS:The incidence of pancreatic cancer in group A was 48.6%and in group B 33.3%.The maximal diameter of tumor mass was significantly larger in group A than that in group B(P0.05).No pathological changes were observed , in the pancreas of group C and other main organs of groups A and B.The positive rates of Ezrin,HGF and C-met were significantly higher in ductal adenocarcinoma than in non- cancerous pancreatic tissues of groups A and B(P0.01).The positive rates of Ezrin,HGF and C-met were significantly higher in ductal adenocarcinoma of group A than those in non- cancerous pancreatic tissues of group A(P0.05),but there was no significant difference in group B(P0.05).The positive rates of Ezrin,HGF and C-met in non-cancerous pancreatic tissues proved mild to severe atypical hyperplasia of the ductal epithelia.The pancreas of group C and 2 cases of fibrosarcoma showed the negative expression of Ezrin,HGF and C-met.There was a trend of consistency in the expression of Ezrin,HGF and C-met in ductal adenocarcinoma(P0.05 or P0.01). CONCLUSIONS:DMBA directly implanted into the parenchyma of the pancreas can produce a model of pancreatic cancer with a high incidence in a short time.TSA might inhibit the carcinogenesis and growth of pancreatic cancer,and its effects may be related to the inhibition of the expression of Ezrin,HGF and C-met during the process.Ezrin,HGF and C-met may have positive effects on the carcinogenesis of rat pancreas.     

Inhibition of KL-6/MUC1 glycosylation limits aggressive progression of pancreatic cancer

AIM:To evaluate the significance of KL-6/MUC1(a type of MUC1)glycosylation in pancreatic cancer progression.METHODS:KL-6/MUC1 expression was detected by immunohistochemistry in 48 patients with pancreatic duct cell carcinoma.The N-/O-glycosylation inhibitors(tunicamycin and benzyl-N-acetyl-α-galactosaminide)were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines,and the effects on KL-6/MUC1 expression,and cell adhesion and invasion were determined.In addition,protein expression of epithelial-mesenchymal transition markers,E-cadherin and vimentin,were evaluated in cells after treatment with glycosylation inhibitors.RESULTS:Overexpression of KL-6/MUC1 was found in all pancreatic cancer tissues,but not in the surrounding normal pancreatic tissues.The expression profile of KL-6/MUC1 was significantly decreased after treatment with the inhibitors.The adhesion and invasive ability of cancer cells were significantly decreased after drug treatment,and increased E-cadherin and decreased vimentin expression were found.CONCLUSION:KL-6/MUC1 glycosylation is involved in pancreatic cancer metastasis and invasion.Therapeutic strategies which target this may help control the aggressive behavior of pancreatic cancer cells.     

β-catenin up-regulates the expression of cyclinD1, c-myc and MMP-7 in human pancreatic cancer： Relationships with carcinogenesis and metastasis

AIM: To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclin D1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of β-catenin expression with cyclinD1, c-myc and MMP-7 expression.METHODS: Using immunohistochemistry, we examined the expression of β-catenin, cyclinD1, c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreatic intraepithelial neoplasia (PanIN) and 10 normal pancreases,respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells.RESULTS: In 10 cases of normal pancreatic tissues,epithelial cells showed equally strong membranous expression of βcatenin protein at the cell-cell boundaries,but the expression of cyclin D1, c-myc and MMP-7 was negative. The expression of βcatenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%),6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12 and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation.The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size,metastasis and one-year survival rate of the pancreatic ancer. The expression of c-myc was not correlated with ize, extent of differentiation, metastasis and 1-year urvival rate, but closely with cell proliferation of pancreatic ancer. The overexpression of MMP-7 was significantly ssociated with metastasis and 1-year survival rate of ancreatic cancer, but not with size, extent of differentiation and cell proliferation. There was a highly significant positive association between abnormal expression of β-catenin and overexpression of cyclinD1, c-myc and MMP-7 not only in PanIN (r = 1.000, 0.845, 0.845), but also in pancreatic cancer (r = 0.437, 0.452, 0.435).CONCLUSION: The abnormal expression of β-catenin plays a key role in the carcinogenesis and progression of human pancreatic carcinoma by up-regulating the expression of cyclinD1, c-myc and MMP-7, resulting in the degradation of extracellular matrix and uncontrolled cell proliferation and differentiation, β-catenin abnormal expression and MMP-7 overexpression may be considered as two useful markers for determining metastasis and prognosis of human pancreatic cancer.     

基质细胞衍生因子/趋化因子受体4轴参与胰腺癌细胞侵袭的体外实验研究

Objective To investigate the expression of chemokine receptor (CXCR)4 in human pancreatic cancer cell lines,and its association with proliferation,adhesion and invasion of pancreatic cancer cells.Methods The CXCR4 mRNA and protein in three pancreatic cancer cell lines were detected by RT-PCR and Western blotting,respectively.Confocal microscopy was used to detect the fluorescence intensity induced by SDF-lα in AsPC-1 cells.MTT test was performed to study the proliferation of pancreatic cancer cells.The invasive ability of pancreatic cell lines was determined by transwell invasion assay kit and the adhesive ability was detected by cell adhesive test in vitro.Results There were expressions of CXCR4 mRNA and protein in different extent in three pancreatic cancer cell lines.The strong expression was seen in AsPC-1 cell line,but weak expression in SW1990 cell line.The CXCR4 was functional expressed on AsPC-1 ceils.SDF-1α improved the proliferation,adhesion and invasion of three pancreatic cancer cell lines,especially in AsPC-1 cell line,while the proliferation in SW1990 cell line was weak.But all above effects of the SDF-1α could be inhibited by AMD3100.Conclasions CXCR4 mRNA and protein were expressed in pancreatic cancer cell lines.The efficacy that SDF-1 can increase the invasive ability of pancreatic cancer ceils through SDF-1/CXCR4 axis is closely related to the expression of CXCR4.     

基质细胞衍生因子/趋化因子受体4轴参与胰腺癌细胞侵袭的体外实验研究

Objective To investigate the expression of chemokine receptor (CXCR)4 in human pancreatic cancer cell lines,and its association with proliferation,adhesion and invasion of pancreatic cancer cells.Methods The CXCR4 mRNA and protein in three pancreatic cancer cell lines were detected by RT-PCR and Western blotting,respectively.Confocal microscopy was used to detect the fluorescence intensity induced by SDF-lα in AsPC-1 cells.MTT test was performed to study the proliferation of pancreatic cancer cells.The invasive ability of pancreatic cell lines was determined by transwell invasion assay kit and the adhesive ability was detected by cell adhesive test in vitro.Results There were expressions of CXCR4 mRNA and protein in different extent in three pancreatic cancer cell lines.The strong expression was seen in AsPC-1 cell line,but weak expression in SW1990 cell line.The CXCR4 was functional expressed on AsPC-1 ceils.SDF-1α improved the proliferation,adhesion and invasion of three pancreatic cancer cell lines,especially in AsPC-1 cell line,while the proliferation in SW1990 cell line was weak.But all above effects of the SDF-1α could be inhibited by AMD3100.Conclasions CXCR4 mRNA and protein were expressed in pancreatic cancer cell lines.The efficacy that SDF-1 can increase the invasive ability of pancreatic cancer ceils through SDF-1/CXCR4 axis is closely related to the expression of CXCR4.     

基质细胞衍生因子/趋化因子受体4轴参与胰腺癌细胞侵袭的体外实验研究

Objective To investigate the expression of chemokine receptor (CXCR)4 in human pancreatic cancer cell lines,and its association with proliferation,adhesion and invasion of pancreatic cancer cells.Methods The CXCR4 mRNA and protein in three pancreatic cancer cell lines were detected by RT-PCR and Western blotting,respectively.Confocal microscopy was used to detect the fluorescence intensity induced by SDF-lα in AsPC-1 cells.MTT test was performed to study the proliferation of pancreatic cancer cells.The invasive ability of pancreatic cell lines was determined by transwell invasion assay kit and the adhesive ability was detected by cell adhesive test in vitro.Results There were expressions of CXCR4 mRNA and protein in different extent in three pancreatic cancer cell lines.The strong expression was seen in AsPC-1 cell line,but weak expression in SW1990 cell line.The CXCR4 was functional expressed on AsPC-1 ceils.SDF-1α improved the proliferation,adhesion and invasion of three pancreatic cancer cell lines,especially in AsPC-1 cell line,while the proliferation in SW1990 cell line was weak.But all above effects of the SDF-1α could be inhibited by AMD3100.Conclasions CXCR4 mRNA and protein were expressed in pancreatic cancer cell lines.The efficacy that SDF-1 can increase the invasive ability of pancreatic cancer ceils through SDF-1/CXCR4 axis is closely related to the expression of CXCR4.     

基质细胞衍生因子/趋化因子受体4轴参与胰腺癌细胞侵袭的体外实验研究

Objective To investigate the expression of chemokine receptor (CXCR)4 in human pancreatic cancer cell lines,and its association with proliferation,adhesion and invasion of pancreatic cancer cells.Methods The CXCR4 mRNA and protein in three pancreatic cancer cell lines were detected by RT-PCR and Western blotting,respectively.Confocal microscopy was used to detect the fluorescence intensity induced by SDF-lα in AsPC-1 cells.MTT test was performed to study the proliferation of pancreatic cancer cells.The invasive ability of pancreatic cell lines was determined by transwell invasion assay kit and the adhesive ability was detected by cell adhesive test in vitro.Results There were expressions of CXCR4 mRNA and protein in different extent in three pancreatic cancer cell lines.The strong expression was seen in AsPC-1 cell line,but weak expression in SW1990 cell line.The CXCR4 was functional expressed on AsPC-1 ceils.SDF-1α improved the proliferation,adhesion and invasion of three pancreatic cancer cell lines,especially in AsPC-1 cell line,while the proliferation in SW1990 cell line was weak.But all above effects of the SDF-1α could be inhibited by AMD3100.Conclasions CXCR4 mRNA and protein were expressed in pancreatic cancer cell lines.The efficacy that SDF-1 can increase the invasive ability of pancreatic cancer ceils through SDF-1/CXCR4 axis is closely related to the expression of CXCR4.     

Correlation between Spiral CT Preoperative Staging of Pancreatic Cancer and PTEN and COX-2 Expression

Background/Aims: The aim of the present study was to evaluate the efficacy of TNM staging of pancreatic cancer by multilayer spiral computed tomography (MSCT) and its correlation with tissue PTEN and COX-2 expression. Methodology: Fifty-two patients with pancreatic cancer had MSCT for TNM staging and PTEN and COX-2 expression were detected in pancreatic cancer tissue by immunohistochemistry. Results: The total accuracy of MSCT was 79.5% in diagnosis of TMN staging of pancreatic cancer, with 73.1% for T staging (70.0% in T1, 65.0% in T2, 82.4% in T3 and 80.0% in T4), 76.9% for N staging (81.8% in N0 and 73.3% in N1) and 88.5% for M staging (89.7% in M0 and 84.6% in M1). The PTEN expression was not related to tumor size (p>0.05) but correlated with T staging, lymph node metastasis and clinical staging (p<0.05). COX-2 expression was not related to tumor size and T staging (p>0.05) but correlated with lymph node metastasis and clinical staging (p<0.05). Conclusions: TNM staging of pancreatic cancer was accurately conducted by MSCT-thin-layer-imaging. The correlation with PTEN and COX-2 expression implied that combined application of both approaches can improve the accuracy of diagnosis and staging in pancreatic cancer.     

胃癌淋巴结转移与VEGF—D、VEGFR-3、LVD的关系

目的探讨胃癌淋巴结转移与血管内皮生长因子D（VEGF—D）、血管内皮生长因子受体3（VEGFR-3）、淋巴管密度（LVD）表达间的关系。方法对59例胃癌术后标本采用免疫组织化学sP法检测VEGF—D表达,用VEGFR-3抗体免疫组织化学sP法标记淋巴管,检测肿瘤组织及正常组织LVD。结果VEGF—D、VEGFR-3在癌组织中表达率分别为59．32％、67．80％,明显高于癌旁不典型增生组织及正常胃黏膜组织（P〈0．05）。癌周组织的LVD表达为（21．29±8．21）,明显高于周边正常组织（P〈0．05）。VEGF—D表达阳性组35例与阴性组24例的LVD分别为（23．15±7．58）和（11．93±5．31）,其差异具有统计学意义（P〈0．05）。VEGF—D、LVD在癌组织中的表达与淋巴结直径、淋巴结分期、浸润深度、TNM分期及分化程度有关（P〈0．05）。结论VEGF．D在胃癌组织中高表达,并与肿瘤的淋巴管形成及淋巴结转移密切相关。     

影响胰头、壶腹部癌患者胰十二指肠切除术后生存的因素

目的分析影响胰头癌、壶腹部癌行胰十二指肠切除术的患者生存期的因素。方法收集1990年1月至2005年6月因胰头癌、壶腹部癌行胰十二指肠切除术的95例患者,有完整随访资料的68例纳入分析。观察的影响因素包括性别,年龄,术前黄疸、GPT、贫血,临床分期,原发肿瘤大小,淋巴结转移,住院期间输血量。Kaplan-Meier法计算累计生存率,单因素分析采用Logrank法,多因素分析采用COX回归模型。结果胰头癌1年、2年、3年生存率分别为37%,12%,12%;壶腹部癌1年、2年、3年生存率分别为60%,38%,31%。单因素分析提示,胰头癌患者的临床分期、肿瘤大小、淋巴结转移及输血量与预后有关(P<0.05);壶腹部癌患者的各观察指标与预后的关系无统计学意义。多因素分析提示输血是胰头癌的独立预后因素;壶腹部癌患者无明确的影响预后的独立因素。结论输血是影响胰头癌预后的独立因素,加强围手术期处理有助改善胰头癌患者的预后。     

胰腺癌组织c-MET表达与循环miR-34a、miR-449水平的相关性

目的 探讨胰腺癌组织织间质表皮转化因子(c-MET)的表达与循环miR-34a、miR-449水平的相关性及其临床意义。方法 收集2015年3月至2017年3月间嘉兴医学院附属第二医院行手术治疗并经病理证实的41例胰腺癌患者的临床资料。通过免疫组织化学染色检测胰腺癌组织及其匹配的癌旁正常胰腺组c-MET表达,根据测定结果将患者分为c-MET阳性组与c-MET阴性组。采集患者手术前和手术后3个月外周血,应用荧光定量PCR法检测循环miR-34a和miR-449水平。分析癌组织c-MET表达与患者临床病理参数、预后及循环miR-34a、miR-449水平的关系。分析循环miR-34a和miR-449水平对胰腺癌TNM分期、淋巴结转移和预后的评估价值。结果 胰腺癌组织c-MET阳性率明显高于癌旁正常组织(63.4%比24.4%),差异有统计学意义(P<0.05)。与c-MET阴性患者比较,c-MET阳性患者TNMⅢ/Ⅳ期者居多(73.1%比33.4%),淋巴结转移率高(76.9%比46.7%),生存时间短(29.5个月比35.0个月),生存率低(38.5%比53.3%),差异均有统计学意义(P值均<0.05)。术前c-MET阳性患者循环miR-34a、miR-449水平明显低于c-MET阴性患者(0.228±0.068比0.524±0.106、0.252±0.063比0.432±0.094,P<0.05),术后c-MET阳性患者循环miR-449水平仍明显低于c-MET阴性患者(0.414±0.088比0.512±0.114,P<0.05),但两组间miR-34a水平的差异无统计学意义。术前循环miR-34a、miR-449水平对胰腺癌TNM分期、淋巴结转移及预后有预测价值(P<0.05)。结论 miR-34a、miR-449靶向结合胰腺癌组织c-MET,有可能成为潜在的胰腺癌标志物。     

超声小探头对结直肠癌术前分期诊断的初步研究

目的：超声小探头（ultrasonic miniprobe,UMP）应用于结、直肠癌术前分期的准确性及可行性。方法：对50例结、直肠癌患者做UMP检查,对准病灶进行全瘤扫描,择最佳影像冻结、摄片,退出UMP,最后做活组织检查,全部病例均行根治术,癌周淋巴结分组编号、装瓶、送病理检查。结果：本组UMP对50例结、直肠浸润深度（T分期）与术后病理浸润深度对比,其准确率T1－T4期分别为75％,80％,88％及67％,T分期的总准确率为84％（P＜0．01）,过高分期5例（10％）,过低分期3例（6％）;N分期,UMP诊断阳性淋巴结（n=22),术后病理（n=28),准确率795,UMP诊断阴性淋巴结（n＝20）,术后病理（n＝22）,准确率91％,总准确率84％（42／50）,敏感性79％,特异性为91％（P＜0．01）。结论：（1）UMP是当前应用于结、直肠癌术前TNM分期最有实用价值的方法之一。肿瘤狭窄患者适应术前分期检查。（2）UMP系高频超声频探头,由于超声穿透深度的限制。对远处转移的M分期是不可能的。（3）UMP对浸润深度及处淋巴结转移有一定的参考价值。并应结合其它影像检查如腹部B超、CT等,扬长弃短,相辅相成,以提高术前分期的准确性及完整性。     

PI3K、AKT、MRP在胰腺癌中的表达及其临床意义

目的 检测PI3K、AKT、MRP蛋白在胰腺癌组织中的表达,探讨它们的临床病理学意义及三者之间的相关性.方法 采用免疫组织化学法检测43例胰腺癌组织、9例CP组织和8例正常胰腺组织中PI3K、AKT、MRP蛋白的表达.结果 PI3K、AKT、MRP在胰腺癌组织中的阳性表达率分别为46.51%、55.81%和39.53%,均高于CP和正常胰腺组织中的表达(P<0.01和P<0.05).PI3K、AKT蛋白表达与胰腺癌的淋巴结转移和TNM分期相关(P<0.05).胰腺癌组织中MRP与PBK均异常表达者为32.56%,均正常表达者为46.51%,两者呈显著正相关(r=0.581,P<0.01);MRP与AKT均异常表达者为32.56%,均正常表达者为37.21%,两者呈显著正相关(r=0.432,P<0.05);PI3K与AKT均异常表达者为37.21%,均正常表达者32.56%,两者呈显著正相关(r=0.306,P<0.05).结论 胰腺癌组织PI3K、AKT和MRP蛋白表达上调,三者呈正相关.P13K和AKT的表达与淋巴结转移及TNM分期有关.     

甲基转移酶3B基因在胰腺癌中的表达

目的 检测胰腺癌组织中甲基转移酶3B(DNMT3B)基因表达,分析其与胰腺癌临床病理参数的关系.方法 应用实时定量PCR和免疫组织化学方法检测42例胰腺癌组织及相应癌旁组织、10例正常胰腺组织中DNMT3B mRNA和蛋白表达.结果 胰腺癌组织、癌旁组织和正常胰腺组织DNM33B mRNA表达量分别为9.4±5.9、1.02±0.71和0,相差非常显著(P<0.05);DNMT3B蛋白表达阳性率分别为83.3%、14.3%和10.0%,相差也非常显著(P<0.01).DNMT3B mRNA表达与I临床分期、肿瘤分化程度和淋巴结转移密切相关(P<0.05或P<0.01);DNMT3B蛋白表达与肿瘤的部位、淋巴结转移有关(P<0.01或P<0.05);DNMT3B mRNA和蛋白表达均与年龄、性别、神经浸润、肿瘤大小、血CEA和CA19-9浓度无关.结论 胰腺癌DNMT3B mRNA和蛋白高表达提示胰腺癌已发生淋巴结转移,预后较差.     

CDK4在胃癌中的表达及临床意义

目的研究CDK4在胃癌组织中的表达与临床病理特征之间的关系。方法采用免疫组化方法检测CDK4在70例胃癌组织及部分相应癌旁组织中的表达,结合患者的性别、年龄、肿瘤大小、部位、分化程度、Borrmann分型、浸润深度、淋巴结转移和TNM分期等临床病理参数进行综合分析。结果胃癌组织和癌旁组织中的CDK4蛋白阳性表达分别为65.71%、18.75%,差异有统计学意义(P0.05)。CDK4在低分化组阳性表达率为78.05%(32/41),中高分化组阳性表达率为48.28%(14/29),两组间比较差异有统计学差异(P0.05,χ2=6.693);CDK4在无淋巴结转移组中阳性表达率为44.83%(13/29),有淋巴结转移组中阳性表达率为80.49%(33/41),两者间比较有显著统计学差异(P0.01,χ2=9.587);CDK4在Ⅰ+Ⅱ期阳性表达率为53.13%(17/32),Ⅲ+Ⅳ期组阳性表达率为76.32%(29/38),两组间比较差异有统计学差异(P0.05,χ2=4.147);CDK4蛋白阳性表达与患者的性别、年龄、肿瘤大小、部位、Borrmann分型、浸润深度均无明显相关(P0.05)。结论 CDK4在胃癌组织中存在着过表达,在评估胃癌的发生、发展中有一定的临床价值。CDK4表达水平与肿瘤组织分化程度、淋巴结有无转移、TNM分期有关。     

Expressions of p53, VEGF C,p21: could they be used in preoperative evaluation of lymph node metastasis of esophageal squamous cell carcinoma?

The prognosis of esophageal squamous cell carcinoma is primarily determined by staging. Although radiological methods have revealed lymph node metastasis preoperatively, these radiological findings cannot be correlated with pathological staging. The aim of this study was to compare the expressions of p53, vascular endothelial growth factor C (VEGF C) and p21 with lymph node metastasis in preoperative endoscopic biopsy and postoperative resection material. Tissue samples were taken from 40 patients who had undergone endoscopic biopsies and radical esophagectomies. The expressions of p53, VEGF C and p21 proteins in these sections were immunohistochemically examined. The expression of each antibody was characterized as a negative or positive reaction according to the pattern and intensity of semiquantitative immunostaining. The staining pattern of antibodies was divided into three groups: < 10% cancer cells were accepted to be (-), 10-50% were (+), heterogenous and > 50% were (+ +), homogenous. For each antibody, statistical correlation with conventional prognostic parameters such as localization, microscopic grade, stage, pathological lymph node metastasis and survival, were investigated. p53 expression was observed in 65.5% (19/29) of lymph node positive cases, whereas p53 was in 50% (20/40) of cases. VEGF C was in 65% (26/40) and p21 was in 15% (6/40) of cases. p53 has the specificity of 90.9% and sensitivity rate of 65.5% in detecting lymph node metastasis and positive predictive value was 95%. Expression of p53 was significantly correlated with stage and lymph node metastasis (P = 0.02 and P = 0.03, respectively). Prediction of lymph node metastasis by p53 was correlated independently and in coexpression with VEGF C (P < 0.01). There was no relation detected between p21 and other parameters. In esophageal squamous cell carcinoma (SCC), p53 and VEGF C expressions were correlated with pathologically positive lymph nodes. When preoperative staging has been insufficient in esophageal carcinoma cases, immunohistochemical analysis of p53 and VEGF C staining in tissues could be an aid to clinicians regarding lymph node metastasis.