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Expression of p53, p16 and COX-2 in pancreatic cancer with tissue microarray

Expression of p53, p16 and COX-2 in pancreatic cancer with tissue microarray

作     者:Lei Xu, You-Ming Li, Chao-Hui Yu, Lan Li, You-Shi Liu, Bao-Feng Zhang, Jing Fang, Qiong Zhou, Ying Hu and Hen-Jun Gao Department of Gastroenterology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China and National Engineering Center for Biochip, Shanghai 200000, China 

作者机构:Department of Gastroenterology First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China. 

出 版 物:《Hepatobiliary & Pancreatic Diseases International》 (国际肝胆胰疾病杂志(英文版))

年 卷 期:2006年第5卷第1期

页      面:138-142页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:The study was supported by a grant from the National 863 program (2002AA2Z2021) 

主  题:pancreatic cancer tissue microarray p53 p16 cyclooxygenase-2 

摘      要:BACKGROUND: Pancreatic cancer development and progression is driven by the accumulation of genetic changes. In this study we constructed tissue microarray containing specimens from pancreatic cancer, adjacent non-cancer tissue and normal tissue to survey the expression of p53, p16 and cyclooxyganase-2 (COX-2). METHODS: Tissue microarray containing 337 specimens from different stages of pancreatic cancer, adjacent noncancer tissue and normal tissues was constructed, and the expression of p53, p16 and COX-2 was assayed by immunohistochemistry to consecutive formalin-fixed tissue microarray sections. RESULTS: The expression of p53, p16 and COX-2 was significantly higher in tumorous tissues than in non-tumorons ones. A significant relationship was observed between p53 and COX-2, or p16 and COX-2. But no obvious correlation was seen between p53 and p16 expressions. Logistic regression analysis showed p53 and COX-2 as dependent predictors in pancreatic carcinogenesis, and a reciprocal relationship to neoplastic progression between p53 and COX-2. CONCLUSION: Combination analysis of p53 and COX-2 may be useful in predicting pancreatic carcinogenesis.

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