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HBV与AFB1诱发树鼠句肝癌前病变过程中癌基因的表达
http://www.100md.com 《中华肝脏病杂志》 1998年第3期
树鼠句γ-谷氨酰转肽酶胰岛素样生长因子Ⅱ肝癌发生,关键词:
HBV与AFB1诱发树鼠句肝癌前病变过程中癌基因的表达

     覃柳亮 苏建家 李瑗 杨春 班克臣 严瑞琪 530021 广西肿瘤防治研究所(覃柳亮、苏建家、李瑗、杨春、班克臣);中山医科大学肿瘤防治中心(严瑞琪) 中华肝脏病杂志 1998 0 0 3


    关键词:树鼠句 γ-谷氨酰转肽酶 胰岛素样生长因子Ⅱ 肝癌发生 期刊 zhgzbzz 0 肝癌专栏 fur -->


    

【摘要】 目的 动态观察黄曲霉毒素B1(AFB1)与乙型肝炎病毒(HBV)诱发树鼠句肝细胞癌(HCC)病变过程,肝癌前病变γ-谷氨酰转肽酶阳性肝细胞灶(GGT阳性灶)和胰岛素样生长因子Ⅱ(IGF-Ⅱ)、p21和p53表达,探讨HCC发生的可能机制。方法 实验动物分4组:A组HBV感染阳性和摄入AFB1;B组HBV阳性;C组摄入AFB1;D组空白对照。采用LSAB、组织化学和原位杂交检测。结果 (1)各实验组肝癌前病变GGT阳性灶数量、大小均明显高于空白组(P<0.05),A组明显大于B、C组(P<0.05);(2)实验第15周,即有IGF-Ⅱ表达,第45周阳性率明显高于第75周(P<0.05);(3)A、B两组动物肝组织中HBsAg阳性率高达92.1%;在树鼠句肝组织中检出HBxAg,阳性率达86.5%。结论 HBV与AFB1协同致树鼠句HCC;HCC发生早期就有癌基因IGF-Ⅱ异常表达。

    

EXPRESSION OF INSULIN-LIKE GROWTH FACTOR II, P53, P21 AND HBxAg IN PRECANCEROUS EVENTS OF HEPATOCARCINOGENESIS INDUCED BY AFB1 AND/OR HBV IN TUPAIA

Qin Liuliang, Su Jianjia, Li Yuan, et al. Department of pathology, Guangxi Cancer Institute Nanning, Guangxi 530021

【Abstract】 Objective The expressions of insulin-like growth factorⅡ(IGF-Ⅱ), p53, p21 and HBxAg during the development of hepatocellular carcinoma (HCC) induced by hepatitis B virus and aflatoxin B1 (AFB1) were studied in animal model of Tupaia. Methods One hundred and twenty Tupaia were divided into 4 groups. Group A with HBV-infected was fed with AFB1; group B was HBV-infected alone; group C was exposed to AFB1 alone and group D without administration of HBV and AFB1 has used as control. The expressions of oncogenes and HBxAg were detected with immunohistochemical assay. Results There was more gamma-glutamytraspeptidase(GGT) positive foci in group A than in group B and C (P<0.05). The expression level of IGF-Ⅱ at the 45th week was higher than at the 75th week in group A, B and C(P<0.05). The expression of IGF-Ⅱ appeared as early as at the 15th week. HBsAg and HBxAg were detected in the HBV-infected groups(group A and B). Conclution Synergistic hepatocarcinogenic effect of HBV infection and AFB1 exposure existed in this model; IGF-Ⅱ was an early marker in hepatocarcinogenesis.

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