Departamento de Matemática e Aplicações , Universidade do Minho , Braga 4710-057 , Portugal ; Centro de Biologia Molecular e Ambiental , Universidade do Minho , Braga 4710-057 , Portugal ; ATP-Group, CMAF , Instituto para a Investigação Interdisciplinar , Lisboa 1649-003 , Portugal.
INESC-ID and Instituto Superior Técnico , Universidade de Lisboa , Taguspark, Porto Salvo, Lisboa 2744-016 , Portugal ; ATP-Group, CMAF , Instituto para a Investigação Interdisciplinar , Lisboa 1649-003 , Portugal.
Interface Focus. 2014 Aug 6;4(4):20140019. doi: 10.1098/rsfs.2014.0019.
The accumulation of somatic mutations, to which the cellular genome is permanently exposed, often leads to cancer. Analysis of any tumour shows that, besides the malignant cells, one finds other 'supporting' cells such as fibroblasts, immune cells of various types and even blood vessels. Together, these cells generate the microenvironment that enables the malignant cell population to grow and ultimately lead to disease. Therefore, understanding the dynamics of tumour growth and response to therapy is incomplete unless the interactions between the malignant cells and normal cells are investigated in the environment in which they take place. The complex interactions between cells in such an ecosystem result from the exchange of information in the form of cytokines- and adhesion-dependent interactions. Such processes impose costs and benefits to the participating cells that may be conveniently recast in the form of a game pay-off matrix. As a result, tumour progression and dynamics can be described in terms of evolutionary game theory (EGT), which provides a convenient framework in which to capture the frequency-dependent nature of ecosystem dynamics. Here, we provide a tutorial review of the central aspects of EGT, establishing a relation with the problem of cancer. Along the way, we also digress on fitness and of ways to compute it. Subsequently, we show how EGT can be applied to the study of the various manifestations and dynamics of multiple myeloma bone disease and its preceding condition known as monoclonal gammopathy of undetermined significance. We translate the complex biochemical signals into costs and benefits of different cell types, thus defining a game pay-off matrix. Then we use the well-known properties of the EGT equations to reduce the number of core parameters that characterize disease evolution. Finally, we provide an interpretation of these core parameters in terms of what their function is in the ecosystem we are describing and generate predictions on the type and timing of interventions that can alter the natural history of these two conditions.
体细胞突变的积累,使细胞基因组永久暴露在外,这往往会导致癌症。对任何肿瘤的分析表明,除了恶性细胞,还会发现其他“支持”细胞,如成纤维细胞、各种类型的免疫细胞,甚至血管。这些细胞共同产生微环境,使恶性细胞群体能够生长,并最终导致疾病。因此,除非在发生的环境中研究恶性细胞和正常细胞之间的相互作用,否则对肿瘤生长和对治疗的反应的理解是不完整的。在这样的生态系统中,细胞之间的复杂相互作用是由于细胞因子和粘附依赖性相互作用形式的信息交换而产生的。这些过程会给参与的细胞带来成本和收益,可以方便地以博弈支付矩阵的形式重新表述。因此,肿瘤的进展和动态可以用进化博弈论(EGT)来描述,它为描述生态系统动态的频率依赖性提供了一个方便的框架。在这里,我们提供了一个关于 EGT 核心方面的教程性综述,建立了与癌症问题的关系。在这个过程中,我们还偏离了关于适合度及其计算方法的讨论。随后,我们展示了如何将 EGT 应用于多发性骨髓瘤骨病及其前驱状态即意义未明的单克隆丙种球蛋白血症的各种表现和动态的研究。我们将复杂的生化信号转化为不同细胞类型的成本和收益,从而定义了一个博弈支付矩阵。然后,我们利用 EGT 方程的已知性质,减少了表征疾病进化的核心参数的数量。最后,我们根据这些核心参数在我们所描述的生态系统中的功能,对其进行解释,并对可能改变这两种情况自然史的干预类型和时间进行预测。