Domschke Pia, Trucu Dumitru, Gerisch Alf, A J Chaplain Mark
Technische Universität Darmstadt, Fachbereich Mathematik, Dolivostr. 15, 64293 Darmstadt, Germany; University of Dundee, Division of Mathematics, Dundee DD1 4HN, Scotland, UK.
University of Dundee, Division of Mathematics, Dundee DD1 4HN, Scotland, UK.
J Theor Biol. 2014 Nov 21;361:41-60. doi: 10.1016/j.jtbi.2014.07.010. Epub 2014 Jul 24.
Cancer invasion, recognised as one of the hallmarks of cancer, is a complex, multiscale phenomenon involving many inter-related genetic, biochemical, cellular and tissue processes at different spatial and temporal scales. Central to invasion is the ability of cancer cells to alter and degrade an extracellular matrix. Combined with abnormal excessive proliferation and migration which is enabled and enhanced by altered cell-cell and cell-matrix adhesion, the cancerous mass can invade the neighbouring tissue. Along with tumour-induced angiogenesis, invasion is a key component of metastatic spread, ultimately leading to the formation of secondary tumours in other parts of the host body. In this paper we explore the spatio-temporal dynamics of a model of cancer invasion, where cell-cell and cell-matrix adhesion is accounted for through non-local interaction terms in a system of partial integro-differential equations. The change of adhesion properties during cancer growth and development is investigated here through time-dependent adhesion characteristics within the cell population as well as those between the cells and the components of the extracellular matrix. Our computational simulation results demonstrate a range of heterogeneous dynamics which are qualitatively similar to the invasive growth patterns observed in a number of different types of cancer, such as tumour infiltrative growth patterns (INF).
癌症侵袭被认为是癌症的标志之一,是一种复杂的多尺度现象,涉及在不同空间和时间尺度上许多相互关联的基因、生化、细胞和组织过程。侵袭的核心是癌细胞改变和降解细胞外基质的能力。结合异常的过度增殖和迁移,这些通过改变的细胞间和细胞与基质的黏附得以实现和增强,癌块能够侵袭邻近组织。连同肿瘤诱导的血管生成,侵袭是转移扩散的关键组成部分,最终导致在宿主身体其他部位形成继发性肿瘤。在本文中,我们探索了一个癌症侵袭模型的时空动态,其中细胞间和细胞与基质的黏附通过偏积分微分方程组中的非局部相互作用项来描述。这里通过细胞群体内以及细胞与细胞外基质成分之间随时间变化的黏附特性,研究了癌症生长和发展过程中黏附特性的变化。我们的计算模拟结果展示了一系列异质动态,这些动态在性质上与在多种不同类型癌症中观察到的侵袭性生长模式相似,例如肿瘤浸润性生长模式(INF)。