Treatment with Imuvert aborts development of chloroleukemia in newborn rats.

J J Jimenez, C A McCall, R E Cirocco, A A Yunis
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Abstract

We have previously demonstrated that the successful transfer of rat chloroleukemia (Mia C51) cells to newborn rats is related to the host's inability to generate adequate levels of differentiation factor (DF). Thus, when the appropriate amount of DF was injected into rats bearing MIA C51 cells, the development of chloroleukemia was aborted. In the present study, we provide evidence that stimulation of endogenous differentiation activity (DA) production by the administration of a biologic response modifier (Imuvert) will like-wise abort the development of chloroleukemia. Imuvert at 50 micrograms/ml had no direct effect on growth, viability, or differentiation of MIA C51 cells. However, when monocytes from young rats or adult rats were stimulated with Imuvert in vivo or in vitro, there was significant increase in DA production. Treatment of young rats with Imuvert aborted the development of chloroleukemia from transplanted MIA C51 cells. It is concluded that stimulation of endogenous DA production may provide a potentially useful approach in the treatment of leukemia.

用Imuvert治疗可终止新生大鼠绿白血病的发展。
我们之前已经证明,大鼠绿白血病(Mia C51)细胞成功转移到新生大鼠体内与宿主无法产生足够水平的分化因子(DF)有关。因此,将适量的DF注射到携带MIA C51细胞的大鼠体内,可以阻止绿白血病的发生。在本研究中,我们提供的证据表明,通过给予生物反应调节剂(Imuvert)刺激内源性分化活性(DA)的产生同样会中止绿白血病的发展。50微克/毫升的剂量对MIA C51细胞的生长、活力或分化没有直接影响。然而,当在体内或体外用Imuvert刺激幼鼠或成年大鼠的单核细胞时,DA的产生显著增加。用Imuvert治疗幼鼠可使移植的MIA C51细胞发生绿白血病。因此,刺激内源性DA的产生可能为白血病的治疗提供一种潜在的有用方法。
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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