Williams S, Mutch D G, Xu L, Collins J L
Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO 63110.
Am J Obstet Gynecol. 1992 Dec;167(6):1870-6. doi: 10.1016/0002-9378(92)91789-d.
Our objective was to study the combined effect of taxol and tumor necrosis factor-alpha on the cytolysis of human ovarian carcinoma cell lines, because taxol has been shown to be active against ovarian carcinoma and has also been shown to increase tumor necrosis factor-alpha release from macrophages.
The combined effect of taxol and tumor necrosis factor-alpha on the cell lines Caov-3, SK-OV-3, NIH:OVCAR-3, and A2780, which are sensitive to the cytolytic effect of tumor necrosis factor-alpha in the presence of inhibitors of protein synthesis, was investigated with a 24-hour chromium 51 release assay.
At therapeutic concentrations taxol caused a significant increase in tumor necrosis factor-alpha-mediated cytolysis of Caov-3 and A2780 (p < or = 0.05). By contrast, taxol caused a decrease in the tumor necrosis factor-alpha-mediated cytolysis of SK-OV-3 and NIH:OVCAR-3 (p < or = 0.01).
These results suggest that ovarian carcinomas have a heterogeneous response to the chemotherapeutic effect of taxol.
我们的目的是研究紫杉醇与肿瘤坏死因子-α对人卵巢癌细胞系细胞溶解作用的联合效应，因为已证明紫杉醇对卵巢癌有活性，并且也已证明它能增加巨噬细胞释放肿瘤坏死因子-α。
采用24小时铬51释放试验，研究在存在蛋白质合成抑制剂的情况下，紫杉醇与肿瘤坏死因子-α对Caov-3、SK-OV-3、NIH:OVCAR-3和A2780细胞系（这些细胞系对肿瘤坏死因子-α的细胞溶解作用敏感）的联合效应。
在治疗浓度下，紫杉醇显著增加了肿瘤坏死因子-α介导的Caov-3和A2780细胞溶解作用（p≤0.05）。相比之下，紫杉醇导致肿瘤坏死因子-α介导的SK-OV-3和NIH:OVCAR-3细胞溶解作用降低（p≤0.01）。
这些结果表明卵巢癌对紫杉醇的化疗效果有不同的反应。
