  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.
