Overall Objectives
Research Program
Application Domains
New Software and Platforms
New Results
Bilateral Contracts and Grants with Industry
Partnerships and Cooperations
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Section: Application Domains

Cancer modelling

Evolution of healthy or cancer cell populations under environmental pressure; drug resistance. Considering cancer as an evolutionary disease – evolution meaning here Darwinian evolution of populations structured according to relevant phenotypes – in collaboration with our biologist partners within the Institut Universitaire de Cancérologie (IUC) of UPMC, we tackle the problem of understanding and limiting a) evolution from pre-malignancy to malignancy in cell populations, and b) in established cancer cell populations, evolution towards (drug-induced) drug resistance. Environmental pressure guiding evolution is of various natures, including signalling molecules induced by the peritumoral stroma (e.g., between a breast tumour and its adipocytic stroma), and anticancer drugs and their effects on both the tumour and its stromal environment. The models we use [59] , [58] [40] are akin to models used in ecology for adaptive dynamics.

Multi-scale modelling of EMT. The major step from a benign tumour that can be eradicated by surgery and an invasive cancer is the development step at which cells detach from the tumour mass and invade individually the surrounding tissue (Weinberg, The biology of cancer, Garland, 2007). The invasion is preceded by a transition (called EMT - epithelial mesenchymal transition) of the cancer phenotype from an epithelial type to a mesenchymal type cell. We so far worked on multi-scale modelling of EMT (Ramis-Conde, Drasdo, Anderson, Chaplain, Biophys. J., 2008), and the step by which invading cancer cells enter blood vessels, called intravasation (Ramis-Conde, Chaplain, Anderson, Drasdo, Phys. Biol. 2009). We now perform in-vitro simulations of cancer cell invasion for Non Small Cell Lung Cancer (NSCLC) having a 5-year survival fraction of about 20%, and for breast cancer. Under development (in collaboration with our biologist partners within the IUC for the experimental part) is also a phenotype-structured PDE model of the interactions between colonies of MCF7 breast cancer and adipocyte stromal support populations.