Yamamoto-Yamaguchi Y, Tomida M, Hozumi M
Department of Chemotherapy, Saitama Cancer Center Research Institute, Japan.
Leuk Res. 1992 Oct;16(10):1025-9. doi: 10.1016/0145-2126(92)90082-i.
Mouse myeloid leukemic M1 cells can be induced to differentiate into macrophages by differentiation-stimulating factor (D-factor)/leukemia inhibitory factor (LIF). We examined the effect of D-factor on the survival times of syngeneic mice implanted with two different clones (T-22 and R-4) of M1 cells. D-factor induced differentiation and suppressed DNA synthesis of sensitive T-22 cells but not resistant R-4 cells in vitro. For in vivo experiments, we used recombinant mouse D-factor (rmD-factor) produced in mammalian cells, which is glycosylated and is more stable in vitro and in vivo than unglycosylated rmD-factor produced in Escherichia coli. Treatment with rmD-factor prolonged the survival times of mice implanted with T-22 cells but not R-4 cells.
小鼠髓性白血病M1细胞可被分化刺激因子（D因子）/白血病抑制因子（LIF）诱导分化为巨噬细胞。我们研究了D因子对植入两种不同克隆（T-22和R-4）M1细胞的同基因小鼠存活时间的影响。在体外，D因子可诱导敏感的T-22细胞分化并抑制其DNA合成，但对耐药的R-4细胞无此作用。在体内实验中，我们使用了在哺乳动物细胞中产生的重组小鼠D因子（rmD因子），它是糖基化的，在体外和体内比在大肠杆菌中产生的未糖基化rmD因子更稳定。用rmD因子处理可延长植入T-22细胞小鼠的存活时间，但对植入R-4细胞的小鼠无效。
