喉癌组织中E-钙黏附素mRNA的表达及意义

目的探讨E-钙黏附素（E-CD）mRNA在喉鳞状细胞癌中的表达及其与喉癌发生发展的关系.方法应用逆转录聚合酶链反应技术对43例喉癌和23例癌旁正常黏膜组织中的E-CD mRNA表达进行检测,并分析检测结果与临床病理因素的关系.结果与癌旁正常黏膜组织相比,喉癌组织中E-CD mRNA表达指数明显降低（P＜0.01）,并与颈淋巴结转移、肿瘤大小（T分期）、临床分期、肿瘤组织分化程度相关,颈淋巴结转移者低于无颈淋巴结转移者（P＜0.01）,T3-4低于T1-2（P＜0.05）,Ⅲ～Ⅳ期低于Ⅰ～Ⅱ期（P＜0.01）,中分化喉癌组织低于高分化组织（P＜0.05）.结论E-CD mRNA低表达与喉癌发生发展相关.     

Indole-3-carbinol enhances anti-proliferative, but not anti-invasive effects of oxaliplatin in colorectal cancer cell lines

The primary aim of this study was to determine whether combination of the chemopreventive agent indole-3-carbinol (I3C) with oxaliplatin would decrease proliferative index and invasive potential of human colorectal tumour cells. Combination of the agents resulted in a 170-fold decrease in proliferative capacity in SW480 and SW620 cell lines, which was approximately 6-fold greater than for oxaliplatin alone. Decreased proliferation was attributed to enhanced S-phase cell cycle arrest for SW480, and increased apoptosis for SW620 cells. The combined agents resulted in significantly increased E-cadherin levels in SW480 cells, and beta-catenin levels in both cell lines (assessed by in-cell westerns). In SW480 cells confocal microscopy revealed an increase in membrane-associated beta-catenin levels, with oxaliplatin treatments enhancing nuclear export and cytoplasmic localisation. In SW620 cells, all treatments increased membrane localisation of E-cadherin. Whilst both oxaliplatin and I3C decreased invasive capacity of SW480 cells, this was not further enhanced by the combined treatment.     

A new mutation of the CDH1 gene in a patient with an aggressive signet-ring cell carcinoma of the stomach

Germline mutations in CDH1, the gene coding for the E-cadherin adhesion protein, are known to cause hereditary diffuse gastric cancer. We identified a new truncating germline mutation (p.Asp538Thrfs*19) in exon 11 of the CDH1 gene in a 41-year-old male with a diffuse gastric cancer. Although he had no parental history of gastric cancer, the co-segregation study in the family detected the same mutation in his healthy 31-year-old brother. The mutation affects one of the extracellular repeat (CAD repeats) domains which is essential for the homophilic binding specificity that directs “E-cadherin” to bind with itself each others. In this case, immunohistochemical analysis showed no expression of E-cadherin in the tumor sample and was a useful prescreening tool to genetic testing. This finding was associated with a poor response to trastuzumab-based treatment.     

Gene expression meta-analysis identifies chromosomal regions and candidate genes involved in breast cancer metastasis

Glypican-3 (GPC3) is a proteoglycan involved in migration, proliferation and cell survival modulation in several tissues. There are many reports demonstrating a downregulation of GPC3 expression in some human tumors, including mesothelioma, ovarian and breast cancer. Previously, we determined that GPC3 reexpression in the murine mammary adenocarcinoma LM3 cells induced an impairment of their in vivo invasive and metastatic capacities together with a higher susceptibility to in vitro apoptosis. Currently, the signaling mechanism of GPC3 is not clear. First, it was speculated that GPC3 regulates the insulin-like growth factor (IGF) signaling system. This hypothesis, however, has been strongly challenged. Recently, several reports indicated that at least in some cell types GPC3 serves as a selective regulator of Wnt signaling. Here we provide new data demonstrating that GPC3 regulates Wnt pathway in the metastatic adenocarcinoma mammary LM3 cell line. We found that GPC3 is able to inhibit canonical Wnt signals involved in cell proliferation and survival, as well as it is able to activate non canonical pathway, which directs cell morphology and migration. This is the first report indicating that breast tumor cell malignant properties can be reverted, at least in part, by GPC3 modulation of Wnt signaling. Our results are consistent with the potential role of GPC3 as a metastasis suppressor. Lydia Puricelli, Elisa Bal de Kier Joffé and María Giselle Peters are the members of the National Council of Scientific and Technical Research (CONICET).     

Bmi-1,a Polycomb Group Protein,Plays an Essential Role in Tumorigenesis and Metastasis

Dysregulation of polycomb group protein Bmi-1 expression has been linked with an invasive phenotype of certain human cancers and poor prognosis of patients; however, the underlying mechanisms are poorly     

E-Cadherin、CD44v6在肾脏恶性肿瘤中的表达及意义

目的探讨E—Cadherin和CD44v6在。肾脏恶性肿瘤中的表达及临床意义。方法选择肾脏恶性肿瘤组织30例和正常肾组织10例,采用免疫组织化学法检测肾脏恶性肿瘤组织和正常肾组织中E—Cadherin、CD44v6的表达,比较两组之间的差异,并分析E—Cadherin和CD44v6与肾脏恶性肿瘤的临床分期、病理分级及淋巴结转移的关系。结果肾脏恶性肿瘤组织E—Cadherin表达显著低于对照组（P〈0．01）,CD44v6表达显著高于对照组（-P〈0．05）。E—Cadherin表达在不同病理分级之间差异不显著（P〉0．05）,CD44v6表达在不同病理分级之间差异显著（P〈0．01）。E—Cadherin、CD44v6表达在不同临床分期之间比较差异有统计学意义（P〈0．05）：E—Cad—herin在有淋巴结转移的肾脏恶性肿瘤组织表达显著低于无淋巴结转移（P〈0．05）。结论E—Cadherin表达下调和CD44v6升高在肾脏恶性肿瘤的发生、发展、浸润等过程中发挥重要的作用。     

蛇毒精氨酸酯酶Agkihpin对人鼻咽癌CNE-2细胞系E-钙粘素表达的影响

目的探讨蛇毒精氨酸酯酶Agkihpin对人鼻咽癌CNE-2细胞系中表皮钙粘素（E-CD）表达的影响,并试图阐明Agkihpin抑制人鼻咽癌CNE-2细胞的机制。方法用不同浓度的Agkihpin处理鼻咽癌细胞株72h后,应用免疫细胞化学、RT—PCR法检测E—CD在CNE一2细胞中的表达。结果不同浓度Agkihpin作用CNE-2细胞72h后E—CD表达均降低,并呈现出一定的浓度依赖效应,显示Agkihpin可显著下调CNE-2细胞中E—CD表达。各加药组与不加Agkihpin纽比较,差异具有统计学意义（P〈0．05）。结论在人低分化鼻咽癌CNE-2细胞系中,Agkihpin能抑制E-CD的表达,并且随浓度的增大有明显的抑制作用。     

EGFR、ER、E-Cadherin在乳腺癌中的表达及其临床意义

目的 观察研究表皮生长因子受体(EGFR)、雌激素(ER) 、E-Cadherin在乳腺癌中的表达及其临床意义.方法 应用免疫组织化学检测77例乳腺癌组织中EGFR、ER、E-Cadherin的表达.结果 77例乳腺癌中,EGFR、ER 、E-Cadherin的阳性表达率分别为29.9％(23/77)、70.1％(54/77)、94.8％(73/77).ER与患者年龄有统计学意义(P＜0.05).结论 ER、E-Cadherin在乳腺癌组织中的高表达与乳腺癌的发生发展密切相关,多种标志物的联合检测可以为乳腺癌的诊疗和评估预后提供新的方法和思路.     

p16蛋白和E-钙粘附蛋白在子宫颈癌中的表达及临床意义

目的　探讨p1 6蛋白及E -钙粘附蛋白 (E -cad)在子宫颈癌中的表达及临床意义。方法　采用单克隆抗体SP免疫组化技术对 5 4例子宫颈癌和 2 0例正常宫颈组织进行p1 6蛋白和E -Cad表达的检测。结果①p1 6蛋白和E -Cad在子宫颈癌和正常宫颈组织中的表达差异有极显著性 ;②p1 6蛋白的表达与子宫颈癌的病理分级和临床分期无显著关联 ,与宫颈癌盆腔淋巴结转移有关 ;③E -Cad的表达与子宫颈癌的病理分级和盆腔淋巴结转移有关 ,但与临床分期无关。结论　p1 6蛋白和E -cad的表达与宫颈癌的发生和进展有一定的相关性 ,p1 6蛋白和E -cad的表达降低或缺失在子宫颈癌的发展过程中有协同作用。检验p1 6蛋白和E -cad的表达可以作为判定子宫颈癌恶性程度的指标之一 ,并为正确估计宫颈癌患者的预后提供依据