Li Yu-Jun, Meng Yun-Xiao, Ji Xiang-Rui
Department of Pathology, Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, China.
Hepatobiliary Pancreat Dis Int. 2003 Aug;2(3):471-7.
To investigate the expressions of E-cadherin and alpha-catenin in pancreatic carcinoma and their relationship with biological behaviors, and clarify the mechanism of invasion and metastasis of pancreatic cancer.
The expressions of E-cadherin and alpha-catenin was examined in 47 patients with infiltrative ductal adenocarcinoma of the pancreas and 12 specimens of normal pancreatic tissues by immunohistochemical technique (PicTure( trade mark ) two-step method). Proliferation cell nuclear antigen (PCNA) was tested as an index of the proliferation degree of pancreatic cancer cells.
The immunoreactivity of E-cadherin and alpha-catenin was expressed by normal ductal and acinar cells with strong membranous staining at the intercellular border in 12 specimens of normal pancreatic tissues. The abnormal rate of E-cadherin expression in pancreatic cancer was 53.2% (25/47), and it was significantly related to differentiation, high proliferation degree and lymph node and liver metastases (P<0.01, 0.05, 0.05 and 0.01, respectively). 61.7% patients with pancreatic cancer (29/47) showed abnormal expression of alpha-catenin. There was a good correlation among alpha-catenin expression, histological grade, and lymph node and liver metastases (P<0.05,0.05 and 0.01, respectively). No significant association was found among abnormal expressions of E-cadherin and alpha-catenin, tumor size, invasion, and 1-year survival rate of patients (P>0.05, all). There was a positive relationship between the expressions of E-cadherin and alpha-catenin in the 47 patients with pancreatic cancer (P<0.01, r=0.88).
Pancreatic cancer likely occurs in case of the inactivation of E-cadherin and alpha-catenin genes and abnormal expression of proteins, which significantly correlate with tumorigenesis, proliferation, differentiation, and lymph node or liver metastasis of pancreatic cancer.
探讨E-钙黏蛋白和α-连环蛋白在胰腺癌中的表达及其与生物学行为的关系，阐明胰腺癌侵袭转移机制。
采用免疫组织化学技术（PicTure（商标）二步法）检测47例胰腺浸润性导管腺癌患者及12例正常胰腺组织标本中E-钙黏蛋白和α-连环蛋白的表达。检测增殖细胞核抗原（PCNA）作为胰腺癌细胞增殖程度的指标。
12例正常胰腺组织标本中，正常导管和腺泡细胞在细胞间边界处呈强膜性染色，表达E-钙黏蛋白和α-连环蛋白的免疫反应性。胰腺癌中E-钙黏蛋白表达异常率为53.2%（25/47），与分化程度、高增殖程度及淋巴结和肝转移显著相关（分别为P<0.01、0.05、0.05和0.01）。61.7%的胰腺癌患者（29/47）α-连环蛋白表达异常。α-连环蛋白表达与组织学分级、淋巴结和肝转移之间存在良好相关性（分别为P<0.05、0.05和0.01）。E-钙黏蛋白和α-连环蛋白异常表达与肿瘤大小、侵袭及患者1年生存率之间未发现显著关联（均P>0.05）。47例胰腺癌患者中E-钙黏蛋白和α-连环蛋白的表达呈正相关（P<0.01，r=0.88）。
胰腺癌可能因E-钙黏蛋白和α-连环蛋白基因失活及蛋白表达异常而发生，这与胰腺癌的发生、增殖、分化及淋巴结或肝转移显著相关。
