AIB1基因在食管鳞状细胞癌发病过程中的作用及临床病理意义
Role of AIB1 gene in development of esophageal squamous cell carcinoma and its clinicopathologic significance
摘要目的 探讨AIB1基因扩增及蛋白表达在食管鳞状细胞癌(ESCC)发病过程中的作用.方法 运用组织芯片技术,通过荧光原位杂交(FISH)与免疫组织化学SABC法对203例ESCC组织中AIB1基因扩增及其编码的AIB1蛋白表达水平进行检测;结合临床病理资料,分析它们之间的相关性.结果 115例ESCC能成功进行FISH检测,其中5例(4.4%)呈现AIB1基因高水平扩增;10例(8.7%)AIB1基因低水平扩增.免疫组织化学检测发现94例(46.3%)ESCC的肿瘤组织出现AIB1蛋白的过度表达;而且AIB1蛋白表达与肿瘤分期有明显相关性,53.7%的T3-4期ESCC(66/123)呈现AIB1蛋白过度表达,远较T1-2期(35.0%,25/80,P=0.008)高.进一步对AIB1基因扩增与蛋白表达进行相关性分析,发现AIB1基因高水平扩增的ESCC全部出现AIB1蛋白过度表达;10例AIB1基因低水平扩增的ESCC中8例出现AIB1蛋白过度表达;剩余100例AIB1基因无扩增的ESCC中,仍有41例呈现AIB1蛋白过度表达.结论 AIB1基因通过基因扩增及其他分子机制导致了其编码蛋白的过度表达,促进了部分亚群ESCC的发生和进展过程.
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abstractsObjective To investigate the role of AIB1 gene in the development of esophageal squamous cell carcinoma(ESCC)and its clinicopathologic significance.Methods Two tissue microarrays,including 203 cases of ESCC,were prepared.Fluorescence in-situ hybridization(FISH)andimmunohistochemistry were performed to detect the amplification of AIB1 gene and expression of its encoded protein in ESCC.The results were correlated with various clinicopathologic parameters.Results In the 203 cases of ESCC studied,FISH was successful in 1 15 cases.Amongst those,amplification/gain of AIBl genewas observed in 15 cases,including high-level amplification in 5 cases(4.3%)and low-level gain in 10cases(8.7%).As for immunohistochemical study,AIB1 protein was overexpressed in 94 cases of ESCC.There was a significant association of AIBl overexpression and tumor staging.AIB1 was overexpressed in 66 of the 123 cases in advanced T stages(T3 to 4),compared with 25 of the 80 cases in early T stages(P=0.008).Those cases with high-level amplification of AIB1 also showed overexpression of its encoded protein.On the other hand,8 of the 10 cases with low-level gain of AIBl showed protein overexpression.The remaining 41 of the 100 cases which did not have AIB1 gene amplification/gain demonstratedoverexpression of AIB1 protein.Conclusion Overexpression of AIB1 protein caused by gene amplification/gain or other molecular mechanisms may play an important role in the development and/or progression of a subset of ESCC.
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