Tannock I
Cancer Res. 1982 Dec;42(12):4921-6.
I have assessed the relative sensitivity of aerobic and hypoxic cells to Adriamycin (ADR) and cyclophosphamide (CY) in the drug-sensitive murine 16/C tumor. The end point used was tumor response to subsequent radiation given under aerobic or acutely hypoxic conditions. Delay in tumor growth following 15 gray radiation alone to approximately 0.4 g tumors was about 3 days longer after aerobic than after hypoxic radiation. Prior treatment with CY had little effect on this difference, implying little selectivity of CY for killing aerobic or hypoxic cells, and the effects of CY and radiation were additive. Treatment with ADR abolished the difference in response to aerobic and hypoxic radiation given from 0.5 to 2 hr after the drug, suggesting that most of the cells which survived treatment with ADR were hypoxic. Difference in response to aerobic and hypoxic radiation at 6 to 24 hr after ADR was equal to or greater than that in non-drug-treated mice, implying rapid reoxygenation after ADR. Experiments on small, nonpalpable tumors with a low proportion of hypoxic cells showed that ADR was slightly more effective than against larger tumors and that some aerobic cells were spared by the drug when the hypoxic fraction was small. Misonidazole is known to be selectively toxic for hypoxic cells, and a high dose of misonidazole gave a small increase in antitumor effects of ADR without increased toxicity. My results suggest that ADR (but not CY) may spare hypoxic cells in a solid tumor and are consistent with limited diffusion of ADR from tumor blood vessels.
我评估了在药物敏感的小鼠16/C肿瘤中,需氧细胞和缺氧细胞对阿霉素(ADR)和环磷酰胺(CY)的相对敏感性。所采用的终点指标是肿瘤对在需氧或急性缺氧条件下给予的后续放疗的反应。单独给予15戈瑞放疗后,约0.4克肿瘤的生长延迟在需氧放疗后比缺氧放疗后长约3天。预先用CY治疗对这种差异影响不大,这意味着CY对杀死需氧或缺氧细胞几乎没有选择性,且CY和放疗的作用是相加的。用ADR治疗消除了给药后0.5至2小时给予的需氧和缺氧放疗反应的差异,这表明经ADR治疗后存活的大多数细胞是缺氧的。ADR给药后6至24小时,需氧和缺氧放疗反应的差异等于或大于未用药小鼠,这意味着ADR给药后有快速的再氧合作用。对缺氧细胞比例低的不可触及的小肿瘤进行的实验表明,ADR对小肿瘤的效果略比对大肿瘤的效果好,并且当缺氧部分较小时,一些需氧细胞可免受该药物的影响。已知米索硝唑对缺氧细胞具有选择性毒性,高剂量的米索硝唑可使ADR的抗肿瘤作用略有增加而不增加毒性。我的结果表明,ADR(而非CY)可能使实体瘤中的缺氧细胞免受影响,这与ADR从肿瘤血管中的有限扩散是一致的。