Hormone independent in vitro erythroid colony formation by mouse bone marrow cells.

K Nooter, R Ghio, K J van der Berg, P A Bentvelzen
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Abstract

B.M. cells of RLV-infected BALB/c mice can proliferate in methylcellulose in the absence of E.P., while normal B.M. cells cannot (12). Not only the more primitive BFU-E shows hormone-independency (18). This phenomenon is in favour of the view that the Rauscher virus induced erythroblastosis is a true neoplasia although transplantation experiments failed so far. The experiments in which transformation in vitro of B.M. cells by RLV is established (19) show that the CFU-E can serve as a target for the virus. Treatment of normal mice with CFA leads to a rapid increase in CFU-E in the bone marrow (18). Splenomegaly of RLV-infected mice is enhanced by CFA-treatment probably due to an increase in targets. Transfection with proviral DNA also can transform the CFU-E of BALB-c mice. This approach allows in vitro studies on the resistence of mouse strains to RLV in vitro. The studies are of interest for the human disease in two aspects. In vitro transformation assays are needed to study the oncogenic potential of putative human leukemia viruses. Furthermore the studies have yielded some new insight in the pathogenesis of virally induced erythroblastosis. This might serve as a model for e.g. acute myeloid leukemia in man.

小鼠骨髓细胞体外不依赖激素的红系集落形成。
在没有e.p.的情况下,rlv感染的BALB/c小鼠的B.M.细胞可以在甲基纤维素中增殖,而正常的B.M.细胞则不能(12)。不仅更原始的BFU-E表现出激素依赖性(18)。这一现象支持劳舍尔病毒诱导的红母细胞病是一种真正的肿瘤的观点,尽管移植实验迄今为止失败。通过RLV在体外转化B.M.细胞的实验(19)表明,CFU-E可以作为病毒的靶标。用CFA治疗正常小鼠可导致骨髓中CFU-E迅速增加(18)。cfa治疗可增强rlv感染小鼠的脾肿大,可能是由于靶点的增加。转染原病毒DNA也能改变BALB-c小鼠的CFU-E。这种方法允许在体外研究小鼠菌株对RLV的耐药性。这些研究对人类疾病有两个方面的意义。需要进行体外转化试验来研究假定的人类白血病病毒的致癌潜力。此外,这些研究还对病毒诱导的红细胞增多症的发病机制有了新的认识。这可以作为人类急性髓性白血病的模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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