A mathematical model of in vitro cancer cell growth and treatment with the antimitotic agent curacin A
A mathematical model of in vitro cancer cell growth and treatment with the antimitotic agent curacin A
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DOI：
10.1016/s0025-5564(00)00065-1
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发表时间：
2001-03-01
影响因子：
4.3
通讯作者：
Panetta, JC
中科院分区：
文献类型：
--
作者：
Kozusko, F;Chen, PH;Panetta, JC
本文提出了一个癌细胞生长和对实验性抗有丝分裂剂Curacin A治疗反应的数学模型。MCF-7/LY 2乳腺癌和A2780卵巢细胞系的未处理生长的速率参数由体外生长研究确定。用2.5、25和50纳摩尔（nM）浓度的Curacin A处理后的后续生长研究用于确定对细胞周期和细胞活力的影响。该模型的常微分方程系统产生一个近似的解析解，预测防止增长所需的最低浓度。该模型表明，当凋亡率大于有丝分裂率时，细胞生长被阻止，并且S-相变率起到放大这种效果的作用。数据的分析表明，curacin A被迅速吸收到两个细胞系中，导致S-相变的增加和M-相变的减少。该模型还表明，与未处理的凋亡率相比，MCF-7/LY 2的凋亡率几乎保持恒定，而A2780的凋亡率在2.5 nM时增加38%，在50 nM时增加59%。(C)2001 Elsevier Science Inc. All rights reserved.
A mathematical model of cancer cell growth and response to treatment with the experimental antimitotic agent curacin A is presented. Rate parameters for the untreated growth of MCF-7/LY2 breast cancer and A2780 ovarian cell lines are determined from in vitro growth studies. Subsequent growth studies following treatments with 2.5, 25 and 50 nanomolar (nM), concentrations of curacin A are used to determine effects on the cell cycle and cell viability. The model's system of ordinary differential equations yields an approximate analytical solution which predicts the minimum concentration necessary to prevent growth. The model shows that cell growth is arrested when the apoptotic rate is greater than the mitotic rate and that the S-phase transition rate acts to amplify this effect. Analysis of the data suggests that curacin A is rapidly absorbed into both cell lines causing an increase in the S-phase transition and a decrease in the M-phase transition. The model also indicates that the rate of apoptosis remains virtually constant for MCF-7/LY2 while that of A2780 increases 38% at 2.5 nM and 59% at 50 nM as compared to the untreated apoptotic rate. (C) 2001 Elsevier Science Inc. All rights reserved.