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Mathematical modelling of cancer cell invasion of tissue: local and non-local models and the effect of adhesion.

机译:癌细胞入侵组织的数学模型:局部和非局部模型以及黏附作用。

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The ability to invade tissue is one of the hallmarks of cancer. Cancer cells achieve this through the secretion of matrix degrading enzymes, cell proliferation, loss of cell-cell adhesion, enhanced cell-matrix adhesion and active migration. Invasion of tissue by the cancer cells is one of the key components in the metastatic cascade, whereby cancer cells spread to distant parts of the host and initiate the growth of secondary tumours (metastases). A better understanding of the complex processes involved in cancer invasion may ultimately lead to treatments being developed which can localise cancer and prevent metastasis. In this paper we formulate a novel continuum model of cancer cell invasion of tissue which explicitly incorporates the important biological processes of cell-cell and cell-matrix adhesion. This is achieved using non-local (integral) terms in a system of partial differential equations where the cells use a so-called "sensing radius"R to detect their environment. We show that in the limitas R-->0 the non-local model converges to a related system of reaction-diffusion-taxis equations. A numerical exploration of this model using computational simulations shows that it can form the basis for future models incorporating more details of the invasion process.
机译:侵入组织的能力是癌症的标志之一。癌细胞通过分泌基质降解酶,细胞增殖,细胞-细胞粘附力丧失,增强的细胞-基质粘附力和主动迁移来实现这一目标。癌细胞对组织的侵袭是转移级联反应的关键组成部分之一,由此癌细胞扩散到宿主的远处并引发继发性肿瘤(转移)的生长。更好地了解与癌症侵袭有关的复杂过程可能最终导致开发出可以定位癌症并预防转移的治疗方法。在本文中,我们制定了一种新型的癌细胞侵袭组织的连续模型,该模型明确纳入了细胞-细胞和细胞-基质粘附的重要生物学过程。这是通过偏微分方程组中的非局部(整数)项来实现的,在该组中,单元格使用所谓的“感应半径” R来检测其环境。我们证明,在极限R> 0时,非局部模型收敛到相关的反应扩散出租车方程组。使用计算仿真对该模型进行的数值研究表明,它可以为包含更多入侵过程细节的未来模型奠定基础。

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