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A mathematical model of tumour angiogenesis: growth regression and regrowth

机译:肿瘤血管生成的数学模型:生长消退和再生长

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摘要

Cancerous tumours have the ability to recruit new blood vessels through a process called angiogenesis. By stimulating vascular growth, tumours get connected to the circulatory system, receive nutrients and open a way to colonize distant organs. Tumour-induced vascular networks become unstable in the absence of tumour angiogenic factors (TAFs). They may undergo alternating stages of growth, regression and regrowth. Following a phase-field methodology, we propose a model of tumour angiogenesis that reproduces the aforementioned features and highlights the importance of vascular regression and regrowth. In contrast with previous theories which focus on vessel remodelling due to the absence of flow, we model an alternative regression mechanism based on the dependency of tumour-induced vascular networks on TAFs. The model captures capillaries at full scale, the plastic dynamics of tumour-induced vessel networks at long time scales, and shows the key role played by filopodia during angiogenesis. The predictions of our model are in agreement with in vivo experiments and may prove useful for the design of antiangiogenic therapies.
机译:癌性肿瘤具有通过称为血管生成的过程募集新血管的能力。通过刺激血管生长,肿瘤与循环系统相连,获得营养,并开辟了一种在远处器官定殖的方式。在没有肿瘤血管生成因子(TAF)的情况下,肿瘤诱导的血管网络变得不稳定。它们可能经历生长,退化和再生长的交替阶段。遵循相场方法,我们提出了一种肿瘤血管生成模型,该模型可再现上述特征并突出显示血管退化和再生长的重要性。与以前的理论(由于缺乏流动而专注于血管重塑)相反,我们基于肿瘤诱导的血管网络对TAF的依赖性对替代的回归机制进行建模。该模型可完整捕获毛细血管,可长时间捕获肿瘤诱导的血管网络的塑性动力学,并显示丝状伪足在血管生成过程中发挥的关键作用。我们模型的预测与体内实验一致,可能被证明可用于抗血管生成疗法的设计。

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