A COMPARISON OF VASCULAR-MEDIATED TUMOR-CELL DEATH BY THE NECROTIZING AGENTS GR63178 AND FLAVONE ACETIC-ACID
A COMPARISON OF VASCULAR-MEDIATED TUMOR-CELL DEATH BY THE NECROTIZING AGENTS GR63178 AND FLAVONE ACETIC-ACID
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DOI：
10.1016/0360-3016(92)90848-c
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发表时间：
1992-01-01
影响因子：
7
通讯作者：
DENEKAMP, J
中科院分区：
文献类型：
--
作者：
HILL, SA;WILLIAMS, KB;DENEKAMP, J
肿瘤损伤的血管成分已被确定为抗癌剂GR63178。在6种小鼠肿瘤模型中比较了该药和黄酮乙酸的坏死性活性及其诱导生长延迟的能力。固定剂量的黄酮乙酸（200mg /kg） 24小时后，所有6种肿瘤类型在组织学上均出现80-100%坏死，尽管生长延迟从3天到79天不等。GR63178 （200 mg/kg）诱导不同程度的坏死（10% ~ 95%），但生长延迟均较小（0 ~ 4天）。这些数据表明，没有肿瘤生长反应不应自动等同于缺乏药物活性。如果不从组织学上评估肿瘤反应，可能会错过具有不同寻常作用机制的药物，尽管它们具有杀死大量肿瘤细胞的潜力。
A vascular component of tumor damage has been identified for the anticancer agent GR63178. The necrotizing activity of this drug and of flavone acetic acid has been compared with their ability to induce growth delay in six murine tumor models. At 24 hr, after a fixed dose of flavone acetic acid (200 mg/kg), all six tumor types appeared 80-100% necrotic histologically, although growth delays ranging from 3 to 79 days were measured. GR63178 (200 mg/kg) induced more variable degrees of necrosis (10 to 95%), but a uniformly small delay in growth (0 to 4 days). These data illustrate that the absence of a tumor-growth response should not be automatically equated with an absence of drug activity. Without assessing tumor response histologically, agents with unusual mechanisms of action may be missed, despite their potential for killing large numbers of tumor cells.