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猴病毒40(SV40)移植抗原(TrAg)的生物学特性。X. SV40转化的小鼠细胞在高反应性C57BL/6小鼠中的致瘤潜力及其与SV40 TrAg、早期蛋白和序列持续性的相关性。

Biology of simian virus 40 (SV40) transplantation antigen (TrAg). X. Tumorigenic potential of mouse cells transformed by SV40 in high responder C57BL/6 mice and correlation with the persistence of SV40 TrAg, early proteins and sequences.

作者信息

Flyer D C, Pretell J, Campbell A E, Liao W S, Tevethia M J, Taylor J M, Tevethia S S

出版信息

Virology. 1983 Nov;131(1):207-20. doi: 10.1016/0042-6822(83)90546-9.

Abstract

Primary mouse embryo fibroblasts of C57Bl/6 origin and cells derived from a tumor induced by polyoma virus in a C57Bl/6 mouse were transformed with SV40. The tumorigenic potential of these cells in normal adult and SV40-immunized mice was correlated with the synthesis of SV40 tumor antigens including the transplantation rejection antigen (TrAg) and with the presence of SV40 early region DNA sequences. Primary cells transformed by SV40 (B6/WT-3) induced tumors in immunocompetent adult syngeneic mice after adaptation in the immunosuppressed host. Passage of these tumor cells (B6/WT-3-T) through SV40-immunized mice resulted in the retention of both T and t antigens and TrAg. However, passage of SV40-transformed polyoma tumor cells through SV40-immunized immunocompetent adult mice but not in nonimmunized mice resulted in the loss of expression of SV40 tumor antigens including TrAg. This loss correlated with the loss of SV40 early region sequences from these double transformed cells. These results demonstrate that the establishment of in vitro SV40-transformed primary mouse cells into a tumor capable of progressive growth in high responder mice does not lead to the selection of variants which have lost the expression of early region DNA sequences.

摘要

源自C57Bl/6的原代小鼠胚胎成纤维细胞以及在C57Bl/6小鼠中由多瘤病毒诱导产生的肿瘤细胞,用SV40进行了转化。这些细胞在正常成年小鼠和经SV40免疫的小鼠中的致瘤潜力与包括移植排斥抗原(TrAg)在内的SV40肿瘤抗原的合成以及SV40早期区域DNA序列的存在相关。经SV40转化的原代细胞(B6/WT - 3)在免疫抑制宿主中适应后,能在具有免疫活性的成年同基因小鼠中诱导肿瘤。这些肿瘤细胞(B6/WT - 3 - T)在经SV40免疫的小鼠中传代后,T抗原、t抗原和TrAg均得以保留。然而,SV40转化的多瘤肿瘤细胞在经SV40免疫的具有免疫活性的成年小鼠中传代,但在未免疫的小鼠中传代则导致包括TrAg在内的SV40肿瘤抗原表达丧失。这种丧失与这些双重转化细胞中SV40早期区域序列的丧失相关。这些结果表明,将体外经SV40转化的原代小鼠细胞建立成能够在高反应性小鼠中进行渐进性生长的肿瘤,并不会导致选择那些丧失早期区域DNA序列表达的变体。

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