Doxorubicin treatment outcomes for non-Hodgkin's lymphomas (NHL) are mathematically modelled and computationally analyzed. The NHL model includes a tumor structure incorporating mature and immature vessels, vascular structural adaptation and NHL cell-cycle kinetics in addition to Doxorubicin pharmacokinetics (PK) and pharmacodynamics (PD). Simulations provide qualitative estimations of the effect of Doxorubicin on high-grade (HG), intermediate-grade (IG) and low-grade (LG) NHL. Simulation results imply that if the interval between successive drug applications is prolonged beyond a certain point, treatment will be inefficient due to effects caused by heterogeneous blood flow in the system.
Abstract. The Hybrid Cellular Automata (HCA) modelling framework can be an efficient approach to a number of biological problems, particularly those which involve the integration of multiple spatial and temporal scales. As such, HCA may become a key modelling tool in the development of the so-called integrative biology. In this paper, we first discuss HCA on a general level and then present results obtained when this approach was implemented in cancer research.
Lipiodol significantly enhanced the uptake of doxorubicin by hepatoblastoma cells in culture. Lipiodol-doxorubicin targeted treatment of hepatoblastoma may improve the intracellular uptake and hence cytotoxicity of doxorubicin in vivo, enabling a reduction in the total dose administered and side-effects.
Abstract. Despite recent advances, treatment of patients with aggressive Non-Hodgkin's lymphoma (NHL 2 ) has yet to be optimally designed. Notwithstanding the contribution of molecular treatments, intensification of chemotherapeutic regimens may still be beneficial. Hoping to aid in the design of intensified chemotherapy, we put forward a mathematical and computational model that analyses the effect of Doxorubicin on NHL over a wide range of patho-physiological conditions. The model represents tumour growth both in diffusion-limited settings, that is, in small avascular tumours and tumour cords, and in perfusion-limited settings, e.g. in well-vascularized tumours. Model simulations indicated the presence of a critical regimen intensity below which treatment will fall short of tumour elimination. Taking this critical intensity into account, we compared two regimen intensification strategies: Dose escalation and regimen densification, i.e. reducing the inter-dosing interval. In the diffusion-limited setting, dose escalation was somewhat more efficient than regimen densification. In the perfusion-limited setting, both intensification strategies yielded similar results. The present study coupled with a realistic myelotoxicity model may add insight on the optimisation of NHL intensified chemotherapy design.
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