Search

The transition from the epithelial to mesenchymal phenotype and its reverse (from mesenchymal to epithelial) are crucial processes necessary for the progression and spread of cancer. In this paper, we investigate how phenotypic switching at the cancer cell level impacts on behaviour at the tissue level, specifically on the emergence of isolated foci of the invading solid tumour mass leading to a multifocal tumour. To this end, we propose a new mathematical model of cancer invasion that includes the influence of cancer cell phenotype on the rate of invasion and metastasis. The implications of model are explored through numerical simulations revealing that the plasticity of tumour cell phenotypes appears to be crucial for disease progression and local invasive spread. The computational simulations show the progression of the invasive spread of a primary cancer reminiscent of in vivo multifocal breast carcinomas, where multiple, synchronous, ipsilateral neoplastic foci are frequently observed and are associated with a poorer patient prognosis.

In the present paper the macroscopic limits of the kinetic model for inter-acting entities (individuals, organisms, cells) are studied. The kinetic model is one-dimensional and entities are characterized by their position and orientation (+/-) with swarming interaction controlled by the sensitivity parameter. The macroscopic limits of the model are considered for solutions close either to the diffusive (isotropic) or to the aligned (swarming) equilibrium states for various sensitivity parameters. In the former case the classical linear difusion equation results whereas in the latter a traveling wave solution does both in the zeroth (`Euler') and frst (`Navier-Stokes') order of approximation.