Hagiwara S, Yuo A, Nagai M, Takezako N, Soda Y, Miwa A, Togawa A, Takaku F
Department of Internal Medicine, Hospital, International Medical Center of Japan.
Rinsho Ketsueki. 1996 Nov;37(11):1259-64.
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.
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。
