The effects of temperature-sensitive Rous sarcoma virus and phorbol diester tumor promoters on cell lineages.
The effects of temperature-sensitive Rous sarcoma virus and phorbol diester tumor promoters on cell lineages.
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温度敏感的劳斯肉瘤病毒和佛波二酯肿瘤启动子对细胞谱系的影响。
DOI：
10.1007/978-3-540-38267-6_22
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发表时间：
1980
影响因子：
--
通讯作者：
West,C
中科院分区：
文献类型：
--
作者：
Holtzer,H;Biehl,J;Pacifici,M;Boettiger,D;Payette,R;West,C
我和我的同事，以及其他许多调查人员（Pierce 1967; Foulds 1969; Pierce and Wallace 1971; Berenblum 1974; Boutwell 1976; Potter 1978）进行了基于以下假设的实验：参与正常细胞转化为恶性细胞的细胞内控制也参与正常细胞之间多样性的产生（Holtzer等人，1972，1974，1975 c）。此外，我们假设这些细胞内控制是允许“克隆的”受精卵、“克隆的”囊胚细胞或“克隆的”肢芽前体细胞在其各自谱系的早期区室中产生多样化后代的机制（Abbott等，1974; Dienstman等，1974; Holtzer 1978）。在所有情况下，基本问题是：一个单一的复制“母”细胞，在量子细胞周期之后，如何产生具有可预测的不同但同样有限的代谢选择的子细胞？一个复制的囊胚细胞，一个复制的红细胞或Friend红白血病细胞（Holtzer et al. 1972，1975 c; Lajtha and斯科菲尔德1974; Weintraub 1975; Holtzer 1978），一种复制型假定成软骨细胞（Holtzer 1978），或复制假定成肌细胞（Holtzer et al. 1975 c; Holtzer 1978）没有选择遵循量子细胞周期，而是分别产生特定不同种类的原肠胚细胞、成红细胞、成软骨细胞和成肌细胞。据推测，作为量子细胞周期的结果，子细胞获得了转录基因组区域的能力，这些区域在它们的母体中不能转录2。同样可能的是，子细胞失去了转录在其母细胞中独特转录的区域的能力。类似地，胚胎癌细胞（Martin 1975）、软骨肉瘤细胞、肝癌细胞或淋巴瘤细胞各自遗传了一组不同的代谢选择，其（1）不仅将这些不同类型的肿瘤细胞彼此区分开，而且（2）将它们与它们的正常母细胞区分开。
My colleagues and I, as well as many other investigators (Pierce 1967; Foulds 1969; Pierce and Wallace 1971; Berenblum 1974; Boutwell 1976; Potter 1978) have performed experiments based on the assumption that those intracellular controls which are involved in the transformation of normal cells into malignant cells are also involved in the generation of diversity among normal cells (Holtzer et al. 1972, 1974, 1975c). In addition, we have assumed that these intracellular controls are the very mechanisms which permit a “cloned” zygote, a “cloned” blastula cell, or a “cloned” limb bud precursor cell in early compartments of their respective lineages to generate diversified progeny (Abbott et al. 1974; Dienstman et al. 1974; Holtzer 1978). In all instances the fundamental question is: How does a single replicating “mother” cell, following a quantal cell cycle, yield daughter(s) with a predictably different, but equally limited, set of metabolic options? A replicating blastula cell, a replicating erythrogenic hematocytoblast or Friend erythroleukemic cell (Holtzer et al. 1972, 1975c; Lajtha and Schofield 1974; Weintraub 1975; Holtzer 1978), a replicating presumptive chondroblast (Holtzer 1978), or a replicating presumptive myoblast (Holtzer et al. 1975c; Holtzer 1978) has no option following a quantal cell cycle, but to yield specifically different kinds of gastrula cells, erythroblasts, chondroblasts, and myoblasts, respectively. Presumably, daughter cells, as a consequence of a quantal cell cycle, acquire the capacity to transcribe regions of the genome that could not be transcribed in their mother2. It is equally likely that the daughter cells lose the capacity to transcribe regions that were uniquely transcribed in their mother cells. Similarly, embryonal carcinoma cells (Martin 1975), chondrosarcoma cells, hepatoma cells, or lymphoma cells have each inherited a different set of metabolic options which (1) not only distinguish these different types of neoplastic cells one from the other, but (2) distinguish them from their normal mother cells.