Metcalf D
Cancer Research Unit, Walter and Eliza Hall Institute, Royal Melbourne Hospital, Victoria, Australia.
Haematol Blood Transfus. 1987;31:16-25. doi: 10.1007/978-3-642-72624-8_4.
Most primary myeloid leukemias are dependent for proliferative stimulation on the glycoprotein colony-stimulating factors. These agents are therefore mandatory co-factors in the development of myeloid leukemia. The CSFs also modify oncogene transcription, and in model leukemogenesis experiments GM-CSF has been shown to be a proto-oncogene. However, most evidence is against an autocrine hypothesis of myeloid leukemia based solely on CSF production by emerging leukemic cells. Because the CSFs also have differentiation commitment actions, they can induce differentiation in myeloid leukemic cells, and G-CSF in particular has an impressive capacity to suppress myeloid leukemic populations by this action. The antagonistic actions of the CSFs on myeloid leukemic cells make it difficult to predict whether they will prove to be useful agents in the management of myeloid leukemias.
大多数原发性髓系白血病的增殖刺激依赖于糖蛋白集落刺激因子。因此,这些因子是髓系白血病发生过程中必不可少的辅助因子。集落刺激因子还能改变癌基因转录,在白血病发生模型实验中,粒细胞-巨噬细胞集落刺激因子已被证明是一种原癌基因。然而,大多数证据反对仅基于新生白血病细胞产生集落刺激因子的髓系白血病自分泌假说。由于集落刺激因子也具有诱导分化的作用,它们可以诱导髓系白血病细胞分化,尤其是粒细胞集落刺激因子通过这种作用具有显著的抑制髓系白血病细胞群的能力。集落刺激因子对髓系白血病细胞的拮抗作用使得难以预测它们是否会被证明是治疗髓系白血病的有效药物。