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肝细胞癌伴门静脉癌栓的基础与临床研究
引用本文:陈孝平,张志伟,张必翔,何松青,张万广,江斌,乔森,潘华锋,史光军,曹斌,黄志勇. 肝细胞癌伴门静脉癌栓的基础与临床研究[J]. 腹部外科, 2003, 16(6): 343-346
作者姓名:陈孝平  张志伟  张必翔  何松青  张万广  江斌  乔森  潘华锋  史光军  曹斌  黄志勇
作者单位:430030,武汉,华中科技大学同济医学院附属同济医院肝脏外科中心
摘    要:目的 探讨肝细胞癌 (HCC)病人门静脉癌栓 (PVTT)不同治疗方法的疗效及PVTT形成的生物学行为与发病机制。方法 回顾性分析 1 995年至 2 0 0 2年间的 2 6 0例HCC伴PVTT病人 ,按不同治疗方法分为 :①肿瘤切除并门静脉取栓组 (S1 =6 2 ) ;②门静脉取栓组 (S2 =5 4 ) ;③介入治疗组 (N1 =4 8) ;④保守治疗组 (N2 =96 )。比较各组间不同的疗效。实验研究对 1 2 3例HCC病人手术切除标本分为 3组 :无PVTT肝癌组 (B)、伴有PVTT的原发癌组 (A1 )及门静脉癌栓组 (A2 )。分析多种基因在癌组织中的表达及在PVTT形成中的意义。结果 S1 组中位生存期为 1 7.2个月 ,术后 1、3、5年生存率分别为 6 7.7%、4 0 .3%和 2 0 .9% ;S2 组中位生存期为 1 2 .6个月 ,术后 1、3、5年生存率分别为33.3%、2 2 .2 %和 7.4 %。N1 组中位生存期为 4 .8个月 ,术后 1、3、5年生存率分别为 2 0 .8%、6 .2 %和0 ;N2 组中位生存期为 1 .5个月 ,1、3、5年生存率分别为 5 .2 %、0、0。各组生存率比较 ,均有显著性差异(P <0 .0 1 )。VEGFmRNA、蛋白的表达率及MVD计数A1 组、A2 组织组均高于B组 ,表达强度A2 组高于A1 组 (P <0 .0 1 ) ;uPA、uPARmRNA及蛋白阳性表达率A2 组和A1 组均高于B组 ,表达强度A2组高于A1 组 (P <0 .0 1 )。E CD蛋白表达

关 键 词:  肝细胞  门静脉  增殖细胞核抗原  胞间粘附分子1  癌基因
修稿时间:2003-10-29

Clinical and experimental study of hepatocellular carcinoma with portal vein tumor thrombus
CHEN Xiao ping,ZHANG Zhi wei,ZHANG Bi xiang,et al.. Clinical and experimental study of hepatocellular carcinoma with portal vein tumor thrombus[J]. Journal of Abdominal Surgery, 2003, 16(6): 343-346
Authors:CHEN Xiao ping  ZHANG Zhi wei  ZHANG Bi xiang  et al.
Affiliation:CHEN Xiao ping,ZHANG Zhi wei,ZHANG Bi xiang,et al.Hepatic Surgery Center,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430030,China
Abstract:Objective To study the value of different treatment methods for hepatocellular carcinoma(HCC)with portal vein tumor thrombus(PVTT)and the molecular mechanisms of PVTT in HCC.Methods 260 HCC patients with PVTT were divided into four groups according to the given therapies:S 1:excision of HCC with removal of PVTT group ( n =62);S 2:removal of PVTT but not excision of HCC group ( n =54);N 1:transcather hepatic arterial chemoembolization(infusion)or/and portal vein infusion group ( n =48);N 2:conservative treatment group ( n =96).The therapeutic effects were compared among the groups.In order to explore the molecular biologic mechanisms of portal vein tumor thrombus in HCC,the resected tumor specimens from 123 cases of HCC were divided into 3 groups as follows:HCC without PVTT(B),HCC with PVTT(A 1)and portal vein tumor thrombus(A 2),respectively.Some genes in the tumor specimens were detected by immunohistochemistry or/and in situ hybridization.Results The 1 ,3 ,5 year survival rate was 67.7% , 43.0% , 20.9% in group S 1, 33.3% , 22.2% , 7.4% in group S 2, 20.8% , 6.2% ,0 in group N 1, 5.2% ,0,0 in group N 2,respectively.There was significant difference among the groups( P < 0.01 ).The expression rate of VEGF,MDV,uPA and uPAR in group A 1 and group A 2 was higher than in group B,and the expression of VEGF,MDV,uPA and uPAR in group A 2 is stronger than in group A 1( P < 0.01 ,respectively).The level of E CD in group A 2 was lower than in group A 1( P < 0.01 ).Conclusion Operation with removal of PVTT is effective treatment for HCC with PVTT,which can prolong the survival rate and improve quality of life.PVTT is formatted by the cooperation of VEGF,uPA,ICAM 1 and PCNA.
Keywords:Carcinoma  hepatocellular  Portal vein  Proliferating cell nuclear antigen  Intercellular adhesion molecule 1  Oncogenes
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