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Expression of hMSH2, hMLH1,transforming growth factor β receptor type Ⅱ, matrix metalloproteinase-7, tissue inhibitor of metalloproteinase-2 and their correlations with the biological behaviors of hereditary nonpolyposis colorectal cancer
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- Author:
- No author available
- Journal Title:
- WORLD CHINESE JOURNAL OF DIGESTOLOGY
- Issue:
- 15
- DOI:
- 10.3969/j.issn.1009-3079.2007.15.011
- Key Word:
- 遗传性非息肉病性大肠癌;散发性大肠癌;错配修复基因;转化生长因子βⅡ型受体;基质金属蛋白酶-7;基质金属蛋白酶组织抑制因子-2;免疫组织化学
Abstract： 目的:探讨遗传性非息肉病性大肠癌(HNPCC)中错配修复基因hMSH2、hMLH1、转化生长因子βⅡ型受体(TβRⅡ)、基质金属蛋白酶-7(MMP-7)、组织抑制因子-2(TIMP-2)表达的相互关系及其与HNPCC特殊生物学行为的关系.方法:应用免疫组织化学染色法检测HNPCC和散发性大肠癌(SCRC)肿瘤组织石蜡标本各30例、正常大肠黏膜石蜡标本8例.观察其hMSH2,hMLH1,TβRⅡ,MMP-7,TIMP-2的表达,并结合临床病理资料综合分析.结果:在HNPCC和SCRC中,hMSH2,hMLH1,TβRⅡ,MMP-7,TIMP-2均与患者的性别、肿瘤大小和部位无关;而与肿瘤的侵犯深度和是否转移密切相关,阳性表达率差异显著(P＜0.05,HNPCC vs sporadic CRC).在HNPCC中,hMSH2和hMLH1 (r=0.835,P=0.000),TβRⅡ与hMSH2 (r=0.592,P=0.001),hMLH1 (r=0.472,P=0.009)和MMP-7(r=0.735,P=0.000)表达均呈明显正相关;而TIMP-2与TβRⅡ(r=-0.582,P=0.001),MMP-7 (r=-0.421,P=0.008)表达呈明显负相关.结论:由于hMSH2,hMLH1突变引起TβRⅡ的失活而诱导的MMP表达减弱和TIMP的下调可能是HNPCC特殊生物学行为的一个原因.
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