Modelling of tissue level carcinogenesis through hybrid, biophysical, and executable approaches

癌症是一个主要的健康问题，三分之一的成年人会在一生中患上这种疾病。然而，在细胞水平上，细胞发展成肿瘤的可能性非常低。细胞通过多种机制的组合来阻止肿瘤的发展，这些机制在不同的尺度上起作用。在单个细胞内，蛋白质和基因形成信号通路，可靠地解释和响应细胞状态和细胞环境，包括来自其他细胞的特定信号。同时，在一个组织内，细胞的运动和位置可以通过限制细胞之间的交流和混合细胞群来增加进一步的控制层。我将建立癌症早期肿瘤形成阶段的数学表示（一个“模型”），将这两种现象联系起来。通过使用该模型进行模拟，我将更多地了解信号和物理成分如何结合起来控制食管上皮细胞的生长和死亡。我将进一步改变和伤害我的模型，以探索这些事件如何导致控制机制的崩溃并导致肿瘤生长。

Cancer is a major health concern, with one in three adults developing the disease over their lifetime. However, on a cellular level, the probability of a cell developing into a tumour is very low. Cells prevent the development of tumours through a combination of mechanisms, which operate over different scales. Within a single cell, proteins and genes form signalling pathways which reliably interpret and respond to both the cell state and the cell environment, including specific signals passed from other cells. At the same time, within a tissue, the movements and locations of cells can add a further layer of control, by limiting the communication between cells and mixing populations of cells. I will build mathematical representations (a “model”) of the early stages of tumour formation in cancer which bridges these two phenomena. By running simulations using this model, I will learn more about how the signalling and physical components combine to control cell growth and death in the oesophageal epithelium. I will further mutate and wound my model, to explore how these events can cause a breakdown of the controlling mechanisms and lead to tumour growth.