Wijeratne Peter A, Vavourakis Vasileios, Hipwell John H, Voutouri Chrysovalantis, Papageorgis Panagiotis, Stylianopoulos Triantafyllos, Evans Andrew, Hawkes David J
Department of Medical Physics and Bioengineering, Centre for Medical Image Computing, University College London, Engineering Front Building, Malet Place, London, WC1E 6BT, UK.
Cancer Biophysics Laboratory, Department of Mechanical and Manufacturing Engineering, University of Cyprus, 1678, Nicosia, Cyprus.
Biomech Model Mechanobiol. 2016 Oct;15(5):1079-90. doi: 10.1007/s10237-015-0745-2. Epub 2015 Nov 12.
Here we introduce a model of solid tumour growth coupled with a multiscale biomechanical description of the tumour microenvironment, which facilitates the explicit simulation of fibre-fibre and tumour-fibre interactions. We hypothesise that such a model, which provides a purely mechanical description of tumour-host interactions, can be used to explain experimental observations of the effect of collagen micromechanics on solid tumour growth. The model was specified to mouse tumour data, and numerical simulations were performed. The multiscale model produced lower stresses than an equivalent continuum-like approach, due to a more realistic remodelling of the collagen microstructure. Furthermore, solid tumour growth was found to cause a passive mechanical realignment of fibres at the tumour boundary from a random to a circumferential orientation. This is in accordance with experimental observations, thus demonstrating that such a response can be explained as purely mechanical. Finally, peritumoural fibre network anisotropy was found to produce anisotropic tumour morphology. The dependency of tumour morphology on the peritumoural microstructure was reduced by adding a load-bearing non-collagenous component to the fibre network constitutive equation.
在此，我们介绍一种实体肿瘤生长模型，该模型与肿瘤微环境的多尺度生物力学描述相结合，有助于对纤维-纤维和肿瘤-纤维相互作用进行显式模拟。我们假设，这样一个提供肿瘤-宿主相互作用纯力学描述的模型，可用于解释关于胶原微力学对实体肿瘤生长影响的实验观察结果。该模型针对小鼠肿瘤数据进行了设定，并进行了数值模拟。由于对胶原微观结构进行了更现实的重塑，多尺度模型产生的应力低于等效的类连续介质方法。此外，发现实体肿瘤生长会导致肿瘤边界处的纤维从随机取向被动机械重排为圆周取向。这与实验观察结果一致，从而表明这种反应可解释为纯力学反应。最后，发现肿瘤周围纤维网络各向异性会产生各向异性肿瘤形态。通过在纤维网络本构方程中添加承载非胶原成分，肿瘤形态对肿瘤周围微观结构的依赖性降低。
