摘要
目的:探讨EphA 2蛋白和KAI 1蛋白的表达与膀胱移行细胞癌发生及浸润转移的关系以及两者表达的相关性。方法:采用免疫组织化学SP法,检测EphA 2蛋白和KAI 1蛋白在88例膀胱移行细胞癌组织及76例相应癌旁正常膀胱黏膜中的表达。结果:EphA 2蛋白在癌组织中的表达明显高于其癌旁正常黏膜(P<0.01);随着膀胱癌病理分级的升高,EphA 2蛋白的表达逐渐增加(P<0.05);在浸润性膀胱癌中的表达明显高于表浅性膀胱癌患者(P<0.05);有淋巴结转移组的表达明显高于无淋巴结转移组(P<0.05)。KAI 1蛋白在癌组织中的表达明显低于癌旁正常膀胱黏膜(P<0.01);随着膀胱癌病理分级的升高,KAI1蛋白的表达逐渐减少(P<0.01);KAI 1在浸润性膀胱癌中的表达明显低于表浅性膀胱癌患者(P<0.05);有淋巴结转移组的表达明显低于无淋巴结转移组(P<0.05)。EphA 2蛋白和KAI 1蛋白的表达在有淋巴结转移的患者中呈显著负相关(P<0.05)。结论:EphA 2蛋白的高表达和KAI 1蛋白的低表达与膀胱移行细胞癌的发生及浸润转移有关。
Objective:To investigate the association of EphA 2 and KAI 1 protein expressions with the occurrence, invasion, and metastasis of bladder transitional cell carcinoma tissues (BTCC).Methods:The expressions of EphA 2 and KAI 1 proteins were determined by immunohistochemical SP method in 88 cases of BTCC tissues and 76 cases of pericancerous normal bladder tissues.Results:The expression of EphA 2 protein was significantly higher in BTCC tissues than in adjacent normal tissues (P〈0.01). The expression of EphA 2 protein was gradually increased with the elevation of pathological grades of BTCC. The positive rate of EphA 2 expression was significantly higher in deeply infiltrating BTCC than superficially infiltrating BTCC (P〈0.05). It was significantly higher in the group with lymph node metastasis than those without lymph node metastasis (P〈0.05). The expression of KAI 1 protein was significantly lower in BTCC tissues than in adjacent normal tissues (P〈0.01). The expression of KAI 1 was gradually decreased with the elevation of pathological grades of BTCC. The positive rate of KAI 1 expression was significantly lower in deeply infiltrating BTCC than in superficially infiltrating BTCC (P〈0.05). It was significantly lower in the BTCC with lymph node metastasis than those without lymph node metastasis (P〈0.05). A significantly negative correlation was observed between the expression of EphA 2 and that of KAI 1 in BTCC tissues with lymph node metastasis (P〈0.05). Conclusion:Overexpression of EphA 2 and weak expression of KAI 1 may be involved in the tumorigenesis, infiltration, and migration of BTCC.
出处
《肿瘤》
CAS
CSCD
北大核心
2008年第2期142-145,共4页
Tumor
基金
宜昌市2006年医疗卫生科技计划项目(编号:A06403)