Speaker
Description
In this talk we illustrate two-interrelated models of, respectively, onset of tumor angiogenesis \cite{m1} and of the effect of an antiangiogenesis therapy \cite{m1}. The key component of the model is a chemotactic mechanism (CM) for new vessel cells sprouting induced by pro-angiogenic factors secreted by the tumor. Our approach is based on a statistical mechanics and it takes into the account both the bias induced by the angiogenic factor gradient and the stochastic changes of the velocity direction. Another distinguishing feature is the spatiotemporal dynamics of tumor-produced lactate.
We first simulated the current recommended drug schedules. The simulations suggests that: i) the therapy is only able to decelerate the tumor growth; ii) a small but not negligible amount of tumor cells situated close to the advancing tumor front is observed; ii) the effect of therapy on growth velocity is strongly delayed w.r.t. the therapy start
We also simulated the effect of alternative drug doses per bolus.
The simulations showed that: i) an increase in the drug dose is sublinearly effective; ii) even significant reductions of doses obtain satisfactory therapeutic results.
Bibliography
@article{m1,
title={Angiogenesis and vessel co-option in a mathematical model of diffusive tumor growth: the role of chemotaxis},
author={Gandolfi, Alberto and De Franciscis, S and d’Onofrio, A and Fasano, A and Sinisgalli, C},
journal={Journal of Theoretical Biology},
volume={512},
pages={110526},
year={2021}
}
@article{m2,
title={Angiogenesis and vessel co-option in a mathematical model of diffusive tumor growth: the role of chemotaxis}, author={d’Onofrio, A and Fasano, A and Papa, F and Sinisgalli, C},
journal={Submitted},
year={2026} }
