病毒肿瘤学作为免疫肿瘤学教唆者的数学模型

Tyler Cassidy;Antony R Humphries
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引用次数: 13

摘要

我们开发并分析了肿瘤-免疫相互作用的数学模型,该模型通过使用分布式延迟微分方程明确地将肿瘤细胞周期持续时间的异质性纳入其中。我们得到了无癌平衡局部稳定的充分必要条件,其中肿瘤-免疫相互作用的数量完全表征了疾病的进展。与免疫编辑假说一致,我们表明减少肿瘤免疫相互作用导致肿瘤扩张。最后,通过模拟数学模型,我们表明肿瘤免疫相互作用的强度决定了病毒治疗的长期成功或失败。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A mathematical model of viral oncology as an immuno-oncology instigator
We develop and analyse a mathematical model of tumour–immune interaction that explicitly incorporates heterogeneity in tumour cell cycle duration by using a distributed delay differential equation. We derive a necessary and sufficient condition for local stability of the cancer-free equilibrium in which the amount of tumour–immune interaction completely characterizes disease progression. Consistent with the immunoediting hypothesis, we show that decreasing tumour–immune interaction leads to tumour expansion. Finally, by simulating the mathematical model, we show that the strength of tumour–immune interaction determines the long-term success or failure of viral therapy.
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