Hatanaka M, Klein R
J Exp Med. 1979 Nov 1;150(5):1195-201. doi: 10.1084/jem.150.5.1195.
The transformed clonal isolates of Indian muntjac diploid cells by a mouse sarcoma virus, 43-2XV, were tested for tumorigenicity in athymic nude mice. In spite of the indistinguishable transformed morphology, the tumorigenicity exhibited four different patterns: (a) no tumor formation; (b) slowly growing regressive tumor formation; (c) rapidly growing regressive tumor formation; and (d) rapidly growing progressive tumor formation. This demonstrates that the same diploid host cells transformed by the same virus reveal variable patterns of tumorigenic expression and some transformed host cells lack the tumorigenicity entirely. The findings that there are at least two chromosomes and four recombinant sites assigned for the proviral integrations of the sarcoma gene into the Indian muntjac gene (M. Hatanaka, R. Klein, R. Kominami, T. Oikawa, H. Okabe, N. Tsuchida, E. C. Connors, and A. Carrano. Transformation of Indian muntjac diploid cells by the proviral integration of sarcoma gene of a mouse retrovirus. Manuscript in preparation.) lead us to propose a hypothesis that variable expressions of tumorigenicity under the neutral background of immune responses, may arise from variable integrations of the sarcoma gene into the host chromosome.
用小鼠肉瘤病毒43 - 2XV对印度麂二倍体细胞的转化克隆分离株进行了无胸腺裸鼠致瘤性测试。尽管转化后的形态难以区分,但致瘤性表现出四种不同模式:(a) 无肿瘤形成;(b) 缓慢生长的退行性肿瘤形成;(c) 快速生长的退行性肿瘤形成;(d) 快速生长的进行性肿瘤形成。这表明,由同一病毒转化的相同二倍体宿主细胞表现出不同的致瘤表达模式,并且一些转化后的宿主细胞完全缺乏致瘤性。关于肉瘤基因前病毒整合到印度麂基因中至少有两条染色体和四个重组位点的研究结果(M. 羽田、R. 克莱因、R. 小见波、T. 及川、H. 冈部、N. 土田、E. C. 康纳斯和A. 卡拉诺。小鼠逆转录病毒肉瘤基因的前病毒整合对印度麂二倍体细胞的转化。正在准备的手稿。)使我们提出一个假设,即在免疫反应的中性背景下,致瘤性的可变表达可能源于肉瘤基因在宿主染色体上的可变整合。