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Intercellular communication is very important for cell development and allows a group of cells to survive as a population. Cancer cells have a similar behavior, presenting the same mechanisms and characteristics of tissue formation. In this article, we model and simulate the formation of different communication channels that allow an interaction between two cells. This is a first step in order to simulate in the future processes that occur in healthy tissue when normal cells surround a cancer cell and to interrupt the communication, thus preventing the spread of malignancy into these cells. The purpose of this study is to propose key molecules, which can be targeted to allow us to break the communication between cancer cells and surrounding normal cells. The simulation is carried out using a flexible bioinformatics platform that we developed, which is itself based on the metaphor chemistry-based model.

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SummaryApoptotic cell death plays a crucial role in development and homeostasis. This process is driven by mitochondrial permeabilization and activation of caspases. In this paper we adopt a tuple spaces-based modelling and simulation approach, and show how it can be applied to the simulation of this intracellular signalling pathway. Specifically, we are working to explore and to understand the complex interaction patterns of the caspases apoptotic and the mitochondrial role. As a first approximation, using the tuple spacesbased in silico approach, we model and simulate both the extrinsic and intrinsic apoptotic signalling pathways and the interactions between them. During apoptosis, mitochondrial proteins, released from mitochondria to cytosol are decisively involved in the process. If the decision is to die, from this point there is normally no return, cancer cells offer resistance to the mitochondrial induction.