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作 者:张杰[1] 王可深[2] 丛书英 邱法波[4] 王修海[5] 王培林[5]
机构地区:[1]北京大学基础医学院细胞生物学教研室,北京100083 [2]青岛大学医学院预防医学教研室 [3]青岛传染病医院 [4]青岛大学医学院附属医院普外科 [5]青岛大学医学院生物学教研室
出 处:《中华肝脏病杂志》2001年第5期294-296,共3页Chinese Journal of Hepatology
摘 要:目的 探讨原癌基因c-myc扩增、抑癌基因MTS1/p16变异以及HBV感染在人肝细胞癌(HCC)发生发展中的作用。 方法 应用差异PCR结合非变性聚丙烯酰胺凝胶电泳银染及激光扫描(d-PCR-PAGE-Laser)技术检测c-myc基因扩增,应用PCR结合单链构象多态(SSCP)银染法分析MTS1/p16基因变异,PCR检测HBV DNA。 结果 (1)29例配对肝细胞癌、癌旁组织中c-myc基因扩增阳性率分别为44.83%(13/29)和51.72%(15/29),两者差异无显著性,P>0.05;但两者均显著高于肝硬化组织c-myc基因扩增的阳性率8.33%(1/12),P<0.05。(2)只有3例(10.34%,3/29)肝细胞癌中发现MTS1/p16基因纯合性缺失,未发现MTS1/p16基因突变。(3)正常肝脏、肝硬化和肝细胞癌组织中HBV DNA的阳性率分别为14.29%(2/14)、66.67%(8/12)和96.55%(28/29),三者间差异具有高度显著性,P<0.001,并且HBV DNA的阳性率随肝脏病情的加重而增高(b=0.3986, P<0.001)。(4)29例肝细胞癌中c-myc基因扩增和HBV DNA存在与否无关(P<0.01)。 结论 (1)c-myc基因扩增和HBV感染与HCC的发生、发展密切相关,HCC中c-myc基因扩增和HBV感染之间无内在相关性。(2)HCC中MTS1/p16基因纯合性缺失和突变的发生频率较低。Objective To observe the roles of c-myc gene amplification, MTS1/p16 gene alternation, and HBV infection in the pathogenesis and progression of hepatocellular carcinoma (HCC). Methods A d-PCR-PAGE-laser scanning technique was used to define amplifications of c-myc oncogene. Alternations of MTS1/p16 gene exon1 and exon2 were analysed by PCR and single-strand conformation polymorphism (SSCP) silver stain method. HBV-DNA was assayed by PCR. Results (1)The positive rates of c-myc gene amplification of HCCs and their paired non-cancerous liver tissues were 44.83% (13/29) and 51.72% (15/29). The discrepancies between them were not significant (P>0.05), but they were both significantly higher than that of cirrhotic liver tissues (8.33%, 1/12, P<0.05). (2)A total of 3 homozygous deletions and no mutations of MTS1/p16 gene exon1 and exon2 in HCCs were found in the subset of HCCs. (3)The discrepancies of the positive rates of HBV-DNA among normal liver (14.29%, 2/14), cirrhotic liver (66.67%, 8/12) and HCCs (96.55%, 28/29) were significant (P<0.001). Moreover, the HBV-DNA positive rates increased according to the development of liver lesions (b=0.3986, P<0.001). Conclusions (1)C-myc gene amplification and HBV infection are closely related to the development and progression in a subset of HCCs. However, c-myc gene amplification does not correlate with the HBV infection in HCCs. (2)The homozygous deletions and mutations of MTS1/p16 gene are infrequently encountered in the subset of HCCs. [
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