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人巨噬细胞集落刺激因子(M-CSF)与小剂量阿糖胞苷联合治疗骨髓增生异常综合征所致急性非淋巴细胞白血病:M-CSF诱导白血病原始细胞增殖及酪氨酸磷酸化

[Successful treatment of acute non-lymphoblastic leukemia from myelodysplastic syndrome by combination of human macrophage colony-stimulating factor (M-CSF) and low dose cytosine arabinoside: M-CSF-induced proliferation and tyrosine phosphorylation in leukemic blasts].

作者信息

Hagiwara S, Yuo A, Nagai M, Takezako N, Soda Y, Miwa A, Togawa A, Takaku F

机构信息

Department of Internal Medicine, Hospital, International Medical Center of Japan.

出版信息

Rinsho Ketsueki. 1996 Nov;37(11):1259-64.

PMID:8960658
Abstract

An 84-year-old woman was admitted with acute non-lymphoblastic leukemia transformed from myelodysplastic syndrome. We examined the signal transduction of the leukemic blasts. Stimulation of the blasts by macrophage colony-stimulating factor (M-CSF) resulted in tyrosine phosphorylation of several cellular proteins. In vitro proliferation of leukemic blasts was stimulated by M-CSF, but not by granulocyte colony-stimulating factor. Based upon these findings, combined therapy with M-CSF and low dose cytosine arabinoside (ara-C) was successful. After her recovery, we confirmed marked reduction of blasts and disappearance of M-CSF-responsive cells. These results suggest that M-CSF could enhance the cytotoxic effect of ara-C on leukemic blasts via its intracellular signaling pathway linked to proliferation.

摘要

一名84岁女性因骨髓增生异常综合征转化的急性非淋巴细胞白血病入院。我们检测了白血病原始细胞的信号转导。巨噬细胞集落刺激因子(M-CSF)刺激原始细胞会导致几种细胞蛋白的酪氨酸磷酸化。白血病原始细胞的体外增殖受到M-CSF的刺激,但不受粒细胞集落刺激因子的刺激。基于这些发现,M-CSF与小剂量阿糖胞苷(ara-C)的联合治疗取得了成功。她康复后,我们证实原始细胞明显减少,且M-CSF反应性细胞消失。这些结果表明,M-CSF可通过其与增殖相关的细胞内信号通路增强ara-C对白血病原始细胞的细胞毒性作用。

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