Multiscale modelling of tumour growth induced by circadian rhythm disruption in epithelial tissue

TL;DR

This paper introduces a multiscale chemo-mechanical model that simulates how circadian rhythm disruptions can trigger tumor growth in epithelial tissue, highlighting the roles of mechanical and chemical interactions.

Contribution

It presents a novel multiscale model integrating mechanical and chemical factors to simulate tumor development due to circadian rhythm failure in epithelial tissue.

Findings

Reproduces spiral wave and clustering patterns in simulations

Shows mechanical property changes affect invasion and localization

Identifies clustering as conducive to cancer formation

Abstract

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.