DNA CONTENT OF DYSPLASTIC LESIONS IN HUMAN AND RAT LIVER

在初步实验中，用细胞分光光度法对其进行了观察 方法采用小鼠肝细胞结节实验方法，建立小鼠肝细胞结节模型。 诱导-促进方案，具有非整倍体模式DNA含量。自.以来 非整倍体与肿瘤进展有关，很可能其 存在对出现结核的那些结核构成“风险因素”。 目前还没有关于肝细胞中核DNA含量的数据 异型增生，人类的一种类似于啮齿动物肝脏的病变 结节。 建议像以前一样检查大鼠诱导的肝脏结节，使用 细胞分光光度和组织化学方法，以确定：a) 非整倍体与部分肝切除、启动或 启动和促进；b)非整倍体肝癌的比例 所产生的模式；c)“停止实验”和 持续促进非整倍体结节；以及d)可能 非整倍体与细胞的持久性或重塑之间的对应关系 结节。进一步提出，非整倍体是一种致病的危险因素。 恶变；这一假说将得到统计检验 小鼠脾内移植的临床资料分析 癌前结节。人类肝细胞异型增生是一种 类似于一些大鼠肝脏结节的癌前状态也会 在有肝硬变和/或肝癌的尸检病例中，通过 细胞分光光度法检测可能的非整倍体模式DNA 分发。 拟议的实验可能导致：a)未来探索可能的 导致非整倍体核DNA含量的机制：b)较少 对体内试验的限制性但更真实的规定 肝癌的发生；以及c)改善肝活检的预后价值， 关于人类肝病患者发生肝癌的可能性 肝硬变。

In preliminary experiments, it has been observed by cytospectrophotometric methods that a small number of nodules, induced in rat livers by an induction-promotion regimen, have an aneuploid modal DNA content. Since aneuploidy is associated with tumor progression, it is likely that its presence constitutes a "risk factor" for those nodules where it appears. There is no data available on nuclear DNA content in "liver cell dysplasia," a lesion in humans which is analogous to the rodent liver nodule. It is proposed to examine liver nodules induced in rats as before, using cytospectrophotometric and histochemical methods, to determine: a) if aneuploidy is associated with either partial hepatectomy, initiation, or initiation and promotion; b) the proportion of hepatomas with aneuploid pattern generated; c) the comparative effects of "stop experiments" and continuous promotion on aneuploid nodules; and d) the possible correspondence between aneuploidy and persistence or remodelling of the nodules. It is further proposed that aneuploidy is a "risk factor" for malignant transformation; this hypothesis will be tested by statistical analysis of data obtained and by intrasplenic transplantation of preneoplastic nodules. The likelihood that human liver cell dysplasia is a premalignant condition akin to some rat liver nodules will also be evaluated in autopsy cases with liver cirrhosis and/or hepatoma, by cytospectrophotometric detection of possible aneuploid modal DNA distribution. The experiments proposed may lead to: a) future exploration of possible mechanisms resulting in the aneuploid nuclear DNA content; b) less restrictive but more veritable regulations for in vivo tests of hepatocarcinogenesis; and c) improved prognostic value of liver biopsies, regarding the probability of hepatoma in human patients with liver cirrhosis.