The main two pitfalls of therapeutics in clinical oncology, that limit increasing drug doses, are unwanted toxic side effects on healthy cell populations and occurrence of resistance to drugs in cancer cell populations. Depending on the constraint considered in the control problem at stake, toxicity or drug resistance, we present two different ways to model the evolution of proliferating cell populations, healthy and cancer, under the control of anti-cancer drugs. In the first case, we use a McKendrick age-structured model of the cell cycle, whereas in the second case, we use a model of evolutionary dynamics, physiologically structured according to a continuous phenotype standing for drug resistance. In both cases, we mention how drug targets may be chosen so as to accurately represent the effects of cytotoxic and of cytostatic drugs, separately, and how one may consider the problem of optimisation of combined therapies. © 2012 American Institute of Physics.
Modelling targets for anticancer drug control optimization in physiologically structured cell population models / Billy, F.; Clairambault, J.; Fercoq, O.; Lorenzi, T.; Lorz, A.; Perthame, B.. - 1479:(2012), pp. 1323-1326. (Intervento presentato al convegno International Conference of Numerical Analysis and Applied Mathematics, ICNAAM 2012 tenutosi a Kos, grc nel 2012) [10.1063/1.4756399].
Modelling targets for anticancer drug control optimization in physiologically structured cell population models
Lorenzi T.;
2012
Abstract
The main two pitfalls of therapeutics in clinical oncology, that limit increasing drug doses, are unwanted toxic side effects on healthy cell populations and occurrence of resistance to drugs in cancer cell populations. Depending on the constraint considered in the control problem at stake, toxicity or drug resistance, we present two different ways to model the evolution of proliferating cell populations, healthy and cancer, under the control of anti-cancer drugs. In the first case, we use a McKendrick age-structured model of the cell cycle, whereas in the second case, we use a model of evolutionary dynamics, physiologically structured according to a continuous phenotype standing for drug resistance. In both cases, we mention how drug targets may be chosen so as to accurately represent the effects of cytotoxic and of cytostatic drugs, separately, and how one may consider the problem of optimisation of combined therapies. © 2012 American Institute of Physics.File | Dimensione | Formato | |
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https://hdl.handle.net/11583/2870746