CAJ | 학술논문

目的探讨TAP1、TNF-α表达与HBV相关肝细胞癌发生发展的关系.方法采用免疫组织化学技术EnVision方法检测35例HBV相关肝癌组织和10例正常肝组织TAP1、TNF-α的表达,并分析其表达与肝癌发生,及与肝癌病理分级的关系.结果正常肝组织TAP1及TNF-α表达阴性,TAP1在HBV相关肝癌组织表达阳性率为91.4％,与正常肝组织表达比较差异有统计学意义(P＜0.01),TNF-α在HBV相关肝癌组织表达阳性率为60％,与正常肝组织表达相比较差异有统计学意义(P＜0.05),并且分化较好的肝癌组织TNF-α阳性表达率显著高于分化较差者(P＜0.05).结论 HBV相关肝癌组织TAP1相关的MHC-Ⅰ类分子限制的抗原递呈途径可能正常；HBV相关肝癌组织TNF-α表达量与肝癌患病及组织分化程度相关.
목적 탐토TAP1、TNF-α표체여HBV상관간세포암발생발전적관계.방법 채용면역조직화학기술EnVision방법검측35례HBV상관간암조직화10례정상간조직TAP1、TNF-α적표체,병분석기표체여간암발생,급여간암병리분급적관계.결과 정상간조직TAP1급TNF-α표체음성,TAP1재HBV상관간암조직표체양성솔위91.4％,여정상간조직표체비교차이유통계학의의(P＜0.01),TNF-α재HBV상관간암조직표체양성솔위60％,여정상간조직표체상비교차이유통계학의의(P＜0.05),병차분화교호적간암조직TNF-α양성표체솔현저고우분화교차자(P＜0.05).결론 HBV상관간암조직TAP1상관적MHC-Ⅰ류분자한제적항원체정도경가능정상；HBV상관간암조직TNF-α표체량여간암환병급조직분화정도상관.
Objective To explore the association of expression of transporter associated with antigen processing(TAP1),tumor necrosis factor-alpha(TNF-α)with occurrence and development of HBV-related hepatocellular carcinoma(HCC).Methods The expression of TAP1 and TNF-α in 35 liver carcinoma tissues,and 10 normal liver tissues were detected with immunohistochemical EnVision method,The expression and clinical significance of TAP1,TNF-α in HBV-related HCC were analyzed.Furthermore,the association of respective expression quantity with pathological typing of HCC was analyzed.Results The expression of TAP1,TNF-α was negative in hepatocytes of normal liver tissues.91.4％ of HCC tissues expressed TAP1.There was significantly statistical difference in expression of TAP1 between HCC tissues and the normal hepatic tissues(P ＜ 0.05);60％ of HCC tissues expressed TNF-α.There was statistical difference in expression of TNF-α between HCC and the normal hepatic tissues(P ＜ 0.05),and the positive expression rate of TNF-α in well-differenciated HCC tissues was significantly higher than that in poorly-differenciated ones(P ＜ 0.05).Conclusion TAP1-related MHC-Ⅰ restricted antigen processing pathway was possibly normal in HBV-related HCC.The expression quantity of TNF-α was associated with the occurrence and degree of pathological differentiation of HBV-related HCC.