Speaker
Description
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. We investigate how phenotypic switching at the cancer cell level impacts the 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 the model are explored through numerical simulations revealing that the plasticity of tumour cell phenotypes appears crucial for disease progression and local invasive spread [1]. The computational simulations show the progression of the invasive spread of primary cancer reminiscent of in vivo multifocal breast carcinomas, where multiple, synchronous neoplastic foci are frequently observed and are associated with a poorer patient prognosis.
References
[1] "Mathematical modelling of cancer invasion: Phenotypic transitioning provides insight into multifocal foci formation", Z Szymańska, M Lachowicz, N Sfakianakis, MAJ Chaplain, J. Comput. Sci., accepted.
