| Summary: | The realm of this dissertation was to study the regeneration process within the complex sciences and produce an extension of the Shirinifard vascular tumour model which could mimic the behaviour of p53 and the first immune response of the organism. Vascular tumours use the regeneration pathway to acess the oxygen supply and increase the growth rate, being one of the most agressive types of tumour known to date. Studying the process has become increasingly important in the search for new drugs and treatments to combat them. As in vitro and in vivo studies are limited to cell cultures and animal biological models, computer simulations can help by integrating the metabolism of several cell types and several chemicals into one simulation and study their interactions and the emergent properties that arise from the model. The main contribution of this dissertation is the development of an extension of the Shirinifard model, a model of the development of a vascular tumour and its relation with the vasculature, which enables the simulation of the immunity of the organism and the metabolism of cellular tumor antigen p53 and its relation with the Hypoxia Inducible Factor enabling the study of different degrees of functionality of p53 and the correspondent outcomes in the morphology and volume of the tumour, as well as it probability of remission. The model developed reveals typical complex systems features such as its emergent properties of tumour volume and morphology being unable to be predicted by the simple rules that model its constituents, namely cells, chemicals and their interactions. The p53 metabolism has revealed a phase change behaviour in which the values attributed to the chemical determined the outcome of the model
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