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机构地区:[1]同济医科大学超微病理研究室,北京中国医学科学院肿瘤研究所分子肿瘤国家重点实验室
出 处:《肿瘤》1995年第6期462-465,共4页Tumor
摘 要:本文应用cDNA-RNA原位杂交技术和组织化学方法,观察了二乙基亚硝胺(DENA)诱发大鼠肝癌前病灶中c-myc、N-ras癌基因和γ-GT酶的表达。结果表明,c-myc、N-ras的过度表达出现于早期增生的小肝细胞以及变异肝细胞灶、增生结节和腺瘤中,γ-GT酶出现稍晚(诱癌6周),起初在病变中的分布与癌基因相似,而在诱癌12周后,酶改变病灶数较癌基因要多。提示两者表达有相关住,癌基因激活可能诱导γ-GT酶的表达,而且一旦γ-GT基因启动后,则可能不受癌基因活动的影响,同时也表明,并非所有γ-GT酶异常细胞都具有癌变倾向。Using cDNA-RNA in situ hybridization technique and histochemical method,the expression of c-myc,N-ras and γ-GT ase in precancerous change of rat liver induced by diethylnitrosamine was observed.The expression of c-myc,N-ras was enhanced in foci of proliferated small hepatocytes and altered hepatocytes as well as hyperplastic nodules.The γ-GT ase appeared later (6 weeks after DENA administration),and showed a similar distribution as oncogenes.However,after 12 weeks exposed to DENA,the γ-GT ase positive foci was more than that of c-myc's and N-ras.These results indicated that the expression of c-myc and N-ras genes in the lesions appeared to be related to the cellular proliferation status and to the reappearance of γ-GT ase.It might suggest that the overexpression of c-myc and N-ras genes could induce the expression of γ-GT gene,Furthermore,once the γ-GT gene was activated,it's expression would not be influenced by the oncogenes.
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