Mekler L B
Acta Virol. 1975 Nov;19(6):501-8.
The approach to the problem of oncogenesis of tumorigenic viruses is compared and analyzed from the position of the Altshtein-Vogt hypothesis and from that of the general theory of oncogenesis advanced by the present author. In contrast to the hypothesis of Altshtein-Vogt dealing mainly with the problem of oncogene origin, the general theory of oncogenesis not only defines concretely the origin of the oncogene and the essence of its product, but also makes it possible to understand why, when and how integration of the oncogene with the genome of the cell leads to the transformation of the cell into a benign cell and when into a malignant tumour cell. An analysis of the essence of the "oncogene position effect" from this standpoint shows that an integration, similar in its mechanism but differing in polarity, of the genome of other viruses with the cell genome should lead to the formation of a corresponding antiviral stable (life-long) immunity or also to the emergence of pseudoautoimmune disease of the type caused by "slow" viruses.
从阿尔特施泰因-沃格特假说以及作者提出的肿瘤发生一般理论的角度,对致瘤病毒致癌问题的研究方法进行了比较和分析。与主要探讨癌基因起源问题的阿尔特施泰因-沃格特假说不同,肿瘤发生一般理论不仅具体界定了癌基因的起源及其产物的本质,还使得人们能够理解为何、何时以及癌基因如何与细胞基因组整合会导致细胞转化为良性细胞,以及何时会转化为恶性肿瘤细胞。从这一角度对“癌基因位置效应”的本质进行分析表明,其他病毒基因组与细胞基因组以机制相似但极性不同的方式进行整合,应会导致相应抗病毒稳定(终身)免疫的形成,或者也会引发由“慢”病毒引起的那种假自身免疫性疾病。