Evidence for growth heterogeneity among foci with different phenotypes in the population of altered hepatocyte foci induced by a single neonatal treatment with carcinogen.
Evidence for growth heterogeneity among foci with different phenotypes in the population of altered hepatocyte foci induced by a single neonatal treatment with carcinogen.
复制标题
单一新生儿致癌剂治疗诱导的改变肝细胞病灶群体中不同表型病灶之间生长异质性的证据。
DOI：
10.1093/carcin/7.2.191
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发表时间：
1986
期刊：
影响因子：
4.7
通讯作者：
Stevens,FJ
中科院分区：
文献类型：
--
作者：
Peraino,C;Carnes,BA;Stevens,FJ
研究了致癌物诱导的肝细胞改变灶的表型和生长特征之间的关系。雄性和雌性大鼠在出生后1天内单次腹腔注射致癌物（二乙基亚硝胺或苯并[a]芘），并在断奶时开始暴露于饮食促进剂（苯巴比妥）。这些大鼠组，然后杀死的时间间隔，并通过使用系列冷冻切片技术，组织化学染色和计算机辅助图像分析，他们的肝脏进行了检查的病灶表现出各种表型标记。这些程序允许在每个表型复杂性水平（每个病灶的标记数量）内鉴定具有不同特定表型（病灶标记的身份）的病灶并确定其大小。这些数据表明，病灶的增长率不同，就特定的焦点表型内的复杂性水平。这一观察补充了以前的证据病灶生长率和表型复杂性水平之间的直接关系，并表明，观察到的焦点表型的多样性反映了真正的生物多样性的焦点人口。鉴于先前的证据（一）稳定的焦点表型;（二）表型不相似的病灶后，一个单一的致癌物治疗的快速出现;（三）生产的焦点由单一的启动事件，我们建议，每个增殖和表型不同的成员的焦点人口反映了病变的发生在一个独特的遗传位点在启动过程中。
Relationships between phenotypic and growth characteristics of carcinogen-induced altered hepatocyte foci were investigated. Male and female rats were given a single i.p. injection of carcinogen (diethylnitrosamine or benzo[a]pyrene) within 1 day after birth and were exposed to dietary promoter (phenobarbital) beginning at weaning. Groups of these rats were then killed at intervals, and their livers were examined for foci exhibiting various phenotypic markers through the use of serial frozen sectioning techniques, histochemical staining and computer-assisted image analysis. These procedures permitted the identification and sizing of foci with different specific phenotypes (identities of focus markers) within each phenotypic complexity level (number of markers per focus). The data suggest that foci growth rates differ with respect to specific focus phenotypes within complexity levels. This observation complements previous demonstrations of a direct relationship between foci growth rates and levels of phenotypic complexity and indicates that the observed diversity of focus phenotypes reflects true biological diversity within the focus population. Given the prior evidence for (i) the stability of focus phenotypes; (ii) the rapid emergence of phenotypically dissimilar foci following a single carcinogen treatment; and (iii) the production of foci by single initiation events, we suggest that each proliferatively and phenotypically distinct member of the focus population reflects the occurrence of a lesion at a unique genetic locus during initiation.