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We propose a multiscale chemo-mechanical model of cancer tumour development in an epithelial tissue. The model is based on transformation of normal cells into the cancerous state triggered by a local failure of spatial synchronisation of the circadian rhythm. The model includes mechanical interactions and chemical signal exchange between neighbouring cells, as well as division of cells and intercalation, and allows for modification of the respective parameters following transformation into the cancerous state. The numerical simulations reproduce different dephasing patterns - spiral waves and quasistationary clustering, with the latter being conducive to cancer formation. Modification of mechanical properties reproduces distinct behaviour of invasive and localised carcinoma.
Molecular circadian clocks, that are found in all nucleated cells of mammals, are known to dictate rhythms of approximately 24 hours (circa diem) to many physiological processes. This includes metabolism (e.g., temperature, hormonal blood levels) and
Migrating cells choose their preferential direction of motion in response to different signals and stimuli sensed by spanning their external environment. However, the presence of dense fibrous regions, lack of proper substrate, and cell overcrowding
In this paper, we derive an effective macroscale description suitable to describe the growth of biological tissue within a porous tissue-engineering scaffold. As in our recent work (Holden textit{et al.} A multiphase multiscale model for nutrient lim
Cells forming various epithelial tissues have a strikingly universal distribution for the number of their edges. It is generally assumed that this topological feature is predefined by the statistics of individual cell divisions in growing tissue but
During morphogenesis, the shape of a tissue emerges from collective cellular behaviors, which are in part regulated by mechanical and biochemical interactions between cells. Quantification of force and stress is therefore necessary to analyze the mec