Potential usefulness of a cultured glioma cell line induced by Rous sarcoma virus in B10.A mouse as an immunotherapy model.

K Sakamoto, H Hoshino, Y Kiuchi, G Nakano, Y Nagamachi
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Abstract

A cultured glioma cell line, SR-B10.A, which was derived from a brain tumor induced in an adult female B10.A mouse by Rous sarcoma virus (RSV), has been established. The morphological appearance of the tumor produced by s.c. inoculating SR-B10.A cells was analogous to an astrocytoma of human glioma. Glial fibrillary acidic protein as well as S-100 protein was positive in these SR-B10.A tumor cells. A population doubling time of the cultured cells was 18.5 hours. Chromosomal analysis revealed a defect in one of the sex chromosomes. Integration of RSV genome was proven to be positive in SR-B10.A cells. It was possible to generate cytotoxic effector cells in the syngeneic B10.A mouse against SR-B10.A. The tumor-bearing syngeneic hosts harbored a suppressor activity in the splenocytes. Although recombinant human tumor necrosis factor (rH-TNF) had no growth inhibitory effect on the SR-B10.A cells in vitro, the s.c. implanted and growing tumor regressed when rH-TNF was administered intratumorally several times. In addition, this anti-tumor effect was completely abrogated when the host mice were treated with wholebody x-ray irradiation prior to the tumor cells inoculation. In contrast, neither rH-TNF (i.v.) nor cyclophosphamide (i.p.) induced the regression of SR-B10.A, indicating that efficacy of the locally administered rH-TNF is dependent on the host immune mechanism. These results suggest that SR-B10.A is a potentially useful tumor model in evaluating efficacy of immunomodulators.

劳斯肉瘤病毒诱导的B10神经胶质瘤细胞系培养的潜在用途。小鼠作为免疫治疗模型。
培养的神经胶质瘤细胞系SR-B10。A,来源于成年女性B10诱导的脑瘤。小鼠感染劳斯肉瘤病毒(RSV),已建立。sc接种SR-B10后肿瘤的形态形态。A细胞类似于人类神经胶质瘤中的星形细胞瘤。SR-B10阳性表达胶质原纤维酸性蛋白和S-100蛋白。一个肿瘤细胞。培养细胞的群体倍增时间为18.5 h。染色体分析显示其中一条性染色体有缺陷。RSV基因组整合在SR-B10中呈阳性。一个细胞。在同基因B10中有可能产生细胞毒性效应细胞。小鼠抗SR-B10.A。携带肿瘤的同基因宿主在脾细胞中具有抑制活性。重组人肿瘤坏死因子(rH-TNF)对SR-B10无生长抑制作用。rH-TNF多次给药后,体外培养的A细胞、移植的sc和正在生长的肿瘤都出现了退化。此外,如果在肿瘤细胞接种前对宿主小鼠进行全身x射线照射,则这种抗肿瘤作用完全消失。rH-TNF (i.v.)和环磷酰胺(i.p.)均未引起SR-B10的消退。A,表明局部给药rH-TNF的疗效依赖于宿主免疫机制。这些结果表明SR-B10。A是评估免疫调节剂疗效的潜在有用的肿瘤模型。
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