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结直肠腺瘤与腺癌的免疫组化研究:E-钙黏蛋白、Syndecan-1、Ets-1。

An immunohistochemical study of colon adenomas and carcinomas: E-cadherin, Syndecan-1, Ets-1.

机构信息

Department of Anatomy and Embryology, University of Medicine and Pharmacy Târgu-Mureş, Târgu-Mureş, Romania.

出版信息

Pathol Oncol Res. 2009 Dec;15(4):579-87. doi: 10.1007/s12253-009-9157-x. Epub 2009 Mar 1.

Abstract

It is thought that dysregulation of E-cadherin, syndecan-1 (CD138) and Ets-1 is involved in carcinoma development. E-cadherin is an important epithelial cell adhesion molecule; syndecan-1 (CD138) is a regulatory proteoglycan in both cell-cell and cell-matrix adhesion and Ets-1 is a proto-oncogene and transcription factor, which takes part in extracellular matrix remodeling. Our goal was to study the changes in the expression of these molecules during colon carcinoma development and progression. We tested 117 colon adenomas and 149 de novo and ex adenoma carcinomas of the colon, using the Ultravision Polymer system. The positive reaction rate was 100% for E-cadherin, 98.3% for syndecan-1 and 22.4% for Ets-1 in adenomas, while in carcinomas it was 88.5%, 62.4% and 56.3% respectively. We found decreasing expression of E-cadherin and syndecan-1 throughout colon carcinoma progression and an opposite regulation for the Ets-1 protein. Decrease in expression of syndecan-1 is more pronounced in carcinomas compared to E-cadherin. De novo carcinomas have lower E-cadherin and syndecan-1 expression, and higher Ets-1 expression compared to ex adenoma carcinomas. These findings support the hypothesis that there are differences in the carcinogenesis of these tumors.

摘要

据认为,E-钙黏蛋白、 syndecan-1(CD138)和 Ets-1 的失调与癌的发生发展有关。E-钙黏蛋白是一种重要的上皮细胞黏附分子; syndecan-1(CD138)是细胞-细胞和细胞-基质黏附中的调节蛋白聚糖,Ets-1 是原癌基因和转录因子,参与细胞外基质重塑。我们的目标是研究这些分子在结直肠癌发生和发展过程中的表达变化。我们使用 Ultravision 聚合物系统检测了 117 例结肠腺瘤和 149 例新发和腺瘤性结肠癌。E-钙黏蛋白、 syndecan-1 和 Ets-1 在腺瘤中的阳性反应率分别为 100%、98.3%和 22.4%,而在癌中则分别为 88.5%、62.4%和 56.3%。我们发现,随着结肠癌的进展,E-钙黏蛋白和 syndecan-1 的表达逐渐降低,而 Ets-1 蛋白的表达则相反。与 E-钙黏蛋白相比, syndecan-1 在癌中的表达降低更为明显。新发癌的 E-钙黏蛋白和 syndecan-1 表达水平较低,Ets-1 表达水平较高,与腺瘤性癌相比。这些发现支持了这些肿瘤在致癌机制上存在差异的假说。

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