TY - JOUR
T1 - Mathematical modelling of cancer invasion
T2 - phenotypic transitioning provides insight into multifocal foci formation
AU - Szymańska, Zuzanna
AU - Lachowicz, Mirosław
AU - Sfakianakis, Nikolaos
AU - Chaplain, Mark A. J.
N1 - Funding: Z. Szymańska acknowledge the support from the National Science Centre, Poland – grant No. 2017/26/M/ST1/00783. N. Sfakianaki’s scientific visit to the University of Warsaw was partially supported by the Excellence Initiative Research University Programme at the University of Warsaw. M. Lachowicz is happy to acknowledge the support from the New Ideas Grant - ”Równania kinetyczne w opisie zjawisk samoorganizacji” funded by the Excellence Initiative Research University Programme at the University of Warsaw.
PY - 2024/1/1
Y1 - 2024/1/1
N2 - 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.
AB - 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.
KW - Cancer invasion
KW - Phenotypic switching
KW - Epithelial-mesenchymal transition
KW - Invasive foci
KW - Multifocal cancer
U2 - 10.1016/j.jocs.2023.102175
DO - 10.1016/j.jocs.2023.102175
M3 - Article
SN - 0377-0427
VL - 75
JO - Journal of Computational and Applied Mathematics
JF - Journal of Computational and Applied Mathematics
M1 - 102175
ER -
