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慢性粒细胞白血病中的体外集落形成细胞和集落刺激因子

In vitro colony forming cells and colony stimulating factor in chronic granulocytic leukaemia.

作者信息

Goldman J M, Th'ng K H, Lowenthal R M

出版信息

Br J Cancer. 1974 Jul;30(1):1-12. doi: 10.1038/bjc.1974.108.

Abstract

We have used the technique of human haemopoietic cell culture in agar to study the peripheral blood and bone marrow colony forming capacity of 23 patients with Ph(1) + ve chronic granulocytic leukaemia (CGL) before and after treatment. In comparison with normal controls the number of colony forming cells (CFC) is moderately increased (about three-fold) in the bone marrow and enormously increased in the peripheral blood of untreated patients. In the peripheral blood their number in general is related to the total leucocyte count. In patients whose blood counts have been restored to normal by the use of cytotoxic drugs the number of CFC in the peripheral blood is very greatly reduced. In the marrow of treated patients CFC are present in approximately normal numbers. When used as feeder layer sto support the culture of normal bone marrow cells, the peripheral blood leucocytes of untreated patients are a uniformly poor source of colony stimulating factor (CSF) and fractionation experiments suggest that this is not due merely to a relative scarcity of monocytes. After treatment the peripheral blood has normal CSF activity and this is associated with the monocytic cell component. The last data may be explained in either of two ways: it is possible that restoration of the blood of patients with CGL to normal values removes a homeostatic factor suppressing the formation of CSF by functionally normal monocytes, or alternatively treatment with cytotoxic drugs leads to the replacement of defective monocytes by a population of relatively normal CSF producing cells.

摘要

我们运用了琼脂中人造血细胞培养技术,来研究23例Ph(1)阳性慢性粒细胞白血病(CGL)患者治疗前后外周血和骨髓的集落形成能力。与正常对照组相比,未经治疗患者的骨髓中集落形成细胞(CFC)数量适度增加(约三倍),外周血中则大幅增加。在外周血中,其数量总体上与白细胞总数相关。使用细胞毒性药物使血细胞计数恢复正常的患者,外周血中CFC数量大幅减少。治疗后患者的骨髓中CFC数量大致正常。当用作饲养层以支持正常骨髓细胞培养时,未经治疗患者的外周血白细胞是集落刺激因子(CSF)的一致不良来源,分级实验表明这不仅仅是由于单核细胞相对稀缺所致。治疗后外周血具有正常的CSF活性,这与单核细胞成分相关。最后这些数据可以用两种方式中的任何一种来解释:有可能CGL患者的血液恢复到正常值消除了一种抑制功能正常的单核细胞形成CSF的稳态因子,或者 alternatively 用细胞毒性药物治疗导致有缺陷的单核细胞被一群产生相对正常CSF的细胞所替代。

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