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目的检测胰腺癌组织中的CXCR4和β-catenin的表达,并探讨两者的相互关系及其在胰腺癌侵袭和转移中的临床意义。方法应用免疫组化SP法对48例胰腺癌及20例正常胰腺组织中的CXCR4和β-catenin蛋白进行检测,并结合临床资料进行分析,采用Kaplan-Meier法分析目标蛋白的表达与临床预后的关系,2组间的生存率曲线比较的假设检验采用Log-rank法;多因素分析采用Cox比例风险回归模型。结果 CXCR4与β-cate-nin在胰腺癌组织中的表达阳性率分别为85.4%(41/48)和75.0%(36/48)。CXCR4与β-catenin的共表达率为70.8%(34/48)。CXCR4的阳性表达与淋巴结转移、TNM分期有关(P值分别为0.012、0.005),β-catenin的阳性表达与淋巴结转移有关(P=0.047)。Kaplan-Meier生存曲线提示CXCR4阳性表达是胰腺癌预后差的一个指标。Cox多因素方差分析提示CXCR4、TNM分期、淋巴结转移是影响胰腺癌预后的独立因素。结论胰腺癌中CXCR4及β-catenin均异常表达,与胰腺癌的生物学效应密切相关;CXCR4的异常表达可能是胰腺癌侵袭、转移的分子机理之一。
Objective To detect the expression of CXCR4 and β-catenin in pancreatic cancer and to explore their correlation and their clinical significance in the invasion and metastasis of pancreatic cancer. Methods The expressions of CXCR4 and β-catenin in 48 cases of pancreatic cancer and 20 cases of normal pancreatic tissue were detected by immunohistochemical SP method. The expression of CXCR4 and β-catenin were detected by Kaplan-Meier method. The expressions of target protein and clinical prognosis The Log-rank test was used to test the hypothesis of the survival rate curve between two groups. Cox proportional hazards regression model was used for multivariate analysis. Results The positive rates of CXCR4 and β-cate-nin in pancreatic cancer tissues were 85.4% (41/48) and 75.0% (36/48), respectively. The co-expression rate of CXCR4 and β-catenin was 70.8% (34/48). The positive expression of CXCR4 correlated with lymph node metastasis and TNM stage (P = 0.012,0.005, respectively). The positive expression of β-catenin correlated with lymph node metastasis (P = 0.047). Kaplan-Meier survival curves suggest that CXCR4 positive expression is an indicator of poor prognosis in pancreatic cancer. Cox regression analysis indicated that CXCR4, TNM stage and lymph node metastasis were independent prognostic factors in pancreatic cancer. Conclusions The abnormal expression of CXCR4 and β-catenin in pancreatic cancer is closely related to the biological effects of pancreatic cancer. The abnormal expression of CXCR4 may be one of the molecular mechanisms of pancreatic cancer invasion and metastasis.