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肿瘤分化:猿猴病毒40和多瘤病毒与小鼠畸胎瘤细胞在体外的相互作用。

Neoplastic differentiation: interaction of simian virus 40 and polyoma virus with murine teratocarcinoma cells in vitro.

作者信息

Swartzendruber D E, Lehman J M

出版信息

J Cell Physiol. 1975 Apr;85(2 Pt 1):179-87. doi: 10.1002/jcp.1040850204.

Abstract

The host-virus interactions of Simian virus 40 (SV40) and polyoma virus (Py) with cell lines established from a teratocarcinoma were studied. The cells utilized in this study were the multipotential stem cell of the teratocarcinoma, embryonal carcinoma, and differentiated cells derived from embryonal carcinoma. Several lines of differentiated cells were established in vitro which included parietal yolk sac, epithelial, and spindle cell types. Embryonal carcinoma cells are not susceptible to infection by either SV40 or Py virus. However, differentiated cells are susceptible to infection by these viruses. The differentiated cells are permissive for Py virus replication and nonpermissive for SV40. Several continuously growing cell lines have been established from the SV40 infected cultures which express T antigen in 100% of the cells. The results indicate that undifferentiated embryonal carcinoma cells and their differentiated progeny respond quite differently to challenge with these two oncogenic DNA viruses.

摘要

对猴病毒40(SV40)和多瘤病毒(Py)与源自畸胎癌的细胞系之间的宿主-病毒相互作用进行了研究。本研究中使用的细胞是畸胎癌的多能干细胞、胚胎癌细胞以及源自胚胎癌的分化细胞。在体外建立了几种分化细胞系,包括壁层卵黄囊、上皮和梭形细胞类型。胚胎癌细胞不易被SV40或Py病毒感染。然而,分化细胞易被这些病毒感染。分化细胞允许Py病毒复制,但不允许SV40复制。从感染SV40的培养物中建立了几个持续生长的细胞系,这些细胞系在100%的细胞中表达T抗原。结果表明,未分化的胚胎癌细胞及其分化后代对这两种致癌DNA病毒的攻击反应截然不同。

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