Sudilovsky O, Hei T K
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.
Cancer Lett. 1991 Feb;56(2):131-5. doi: 10.1016/0304-3835(91)90087-x.
Since a number of rat hepatocarcinomas are aneuploid, the model DNA content of enzyme-altered foci was determined cytospectrophotometrically, to assess if ploidy changes occur before cancer is established. Male F344 rats treated with diethylnitrosamine and promoted with a choline-deficient, phenobarbital supplemented diet showed in most enzyme-altered foci a multimodal ploidy distribution with diploid, tetraploid and octoploid peaks. A minority of foci, however, exhibited an aneuploid pattern. This change in ploidy reflects irreversible genomic alterations, indicative of tumor progression. Thus, promotion and progression may coexist simultaneously in this model of carcinogenesis, long before hepatomas can be diagnosed.
由于许多大鼠肝癌为非整倍体，采用细胞分光光度法测定酶改变灶的模型DNA含量，以评估在癌症形成之前是否发生了倍性变化。用二乙基亚硝胺处理并用胆碱缺乏、补充苯巴比妥的饮食促进的雄性F344大鼠，在大多数酶改变灶中显示出具有二倍体、四倍体和八倍体峰的多峰倍性分布。然而，少数灶表现出非整倍体模式。这种倍性变化反映了不可逆的基因组改变，表明肿瘤进展。因此，在这个致癌模型中，早在肝癌能够被诊断出来之前，促进和进展可能同时存在。
