肝细胞癌门静脉癌栓形成的分子生物学机制研究

目的 探讨肝细胞癌（HCC）患者门静脉癌栓（PVTT）形成的分子生物学机制。方法 采用免疫组织化学，原位杂交等方法分别对HCC伴有和不伴有PVTT的组织标本252例进行相关指标的检测，分析多种基因在PVTT形成中的意义。标本分为：A组，未发现转移和PVTT的原发肝细胞癌组织，78例；B组，伴PVTT的原发肝细胞癌组织，50例；C组，PVTT，92例；D组，癌旁组织。32例。结果 内皮钙黏附蛋白（E-CD）的表达为癌旁组织（D组）＞伴PVTT的原发癌组织（B组）＞门静脉癌栓组织（C组）；尿激酶型纤溶酶原激活物（uPA）／其受体（uPAR）的表达规律为门静脉癌栓组织（C组）＞伴PVTT的原发癌组织（B组）＞无转移肝癌组织（A组）（P均＜0．01）；增殖细胞核抗原（PCNA）的表达为门静脉癌栓组织（C组）＞伴PVTT的原发癌组织（B组）＞无转移肝癌组织（A组）；血管内皮细胞生长因子（VEGF）表达为门静脉癌栓组织（C组）＞伴PVTT的原发癌组织（B组）＞无转移肝癌组织（A组）（P均＜0．01）。结论PVTT组织中VEGF、PCNA、uPA／uPAR高表达，E-CD低表达为共同参与肝细胞癌门静脉癌栓形成的分子生物学机制。

An experimental study of molecular mechanisms of portal vein tumor thrombus in hepatocellular carcinoma

Objective To study the molecular mechanisms of portal vein tumor thrombus (PVTT) in hepatocellular carcinoma (HCC).Methods 252 samples with or without PVTT were analyzed in some indexes by the methods of immunohistochemistry and in situ hybridization.The 252 HCC patients were divided into 4 groups:Group A:HCC without metastasis and PVTT (n=78);Group B:HCC with PVTT (n=50);Group C:PVTT (n=92);D:Tissues adjacent to HCC (n=32).Results The expression levels of VEGF and uPA/uPAR in groups C and B were higher than in group A (P< 0.01).The protein expression levels were corresponding with those in mRNA.The expression of E-CD in group D was higher than in group B,and higher in group B than in group C (P< 0.01).The expression of PCNA in group C was higher than in group B (P< 0.01),and higher in group B than in group A (P< 0.05).Conclusion The high expression of VEGF,PCNA,uPA/uPAR and low expression of E-CD all play a role in the molecular biology mechanism of PVTT.