Bradley M O, Kohn K W, Sharkey N A, Ewig R A
Cancer Res. 1977 Jul;37(7 Pt 1):2126-31.
Normal human WI-38 cells can be protected from killing by hydroxyurea if proliferation is arrested during drug treatment. This protection was demonstrated both in cells arrested by density-dependent inhibition and by 3'-amino-3'deoxy-N6,N6-dimethyladenosine (puromycin aminonucleoside). In contrast, VA-13 cells (a simian virus 40-transformed clone of WI-38) were not arrested under these conditions, and continued to be sensitive to hydroxyurea. These results suggest that a search for agents that selectively and reversibly inhibit normal cycling human cells might lead to an enhancement of differential tumor toxicity.
如果在药物处理期间细胞增殖被阻断,正常的人类WI-38细胞可免受羟基脲的杀伤作用。在因密度依赖性抑制以及3'-氨基-3'-脱氧-N6,N6-二甲基腺苷(嘌呤霉素氨基核苷)而阻断的细胞中均证实了这种保护作用。相比之下,VA-13细胞(WI-38的猿猴病毒40转化克隆)在这些条件下未被阻断,并继续对羟基脲敏感。这些结果表明,寻找能选择性且可逆地抑制正常循环人类细胞的药物可能会增强肿瘤的差异毒性。