A Single Cell‐Based Model of the Ductal Tumour Microarchitecture
KA Rejniak, RH Dillon - Computational and Mathematical …, 2007 - Wiley Online Library
Computational and Mathematical Methods in Medicine, 2007•Wiley Online Library
The preinvasive intraductal tumours, such as the breast or prostate carcinomas, develop in
many different architectural forms. There are, however, no experimental models explaining
why cancer cells grow in these various configurations. We use a mathematical model to
compare different proliferative conditions that can lead to such distinct microarchitectures. In
order to simulate different scenarios of tumour growth, we employed a single cell‐based
technique that allows us to model development of the whole tumour tissue by focusing on …
many different architectural forms. There are, however, no experimental models explaining
why cancer cells grow in these various configurations. We use a mathematical model to
compare different proliferative conditions that can lead to such distinct microarchitectures. In
order to simulate different scenarios of tumour growth, we employed a single cell‐based
technique that allows us to model development of the whole tumour tissue by focusing on …
The preinvasive intraductal tumours, such as the breast or prostate carcinomas, develop in many different architectural forms. There are, however, no experimental models explaining why cancer cells grow in these various configurations. We use a mathematical model to compare different proliferative conditions that can lead to such distinct microarchitectures. In order to simulate different scenarios of tumour growth, we employed a single cell‐based technique that allows us to model development of the whole tumour tissue by focusing on biomechanical processes of individual cells and on communication between cells and their microenvironment. Formation of four specific intraductal tumour patterns, micropapillary, cribriform, tufting and solid, are presented in this paper together with a discussion on gradual dedifferentiation of ductal epithelial cells that gives rise to these distinct carcinomas. We introduce two versions of our cell‐based model to show that the obtained results do not depend on a particularly chosen cell structure.
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