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A Mathematical Explanation to Tumor's Response to Perfusion and Hypoxic Fraction After Radiation
Y Yan1*, M Kissick1, J Bussink2,S Jacques3, A van der Kogel1, D Campos1, D Zhao1, (1) University of Wisconsin, Madison, WI, (2) Radboud University, Nijmegen, The Netherlands, (3) Oregon Health & Science University, Portland, OR.
SU-E-T-6 Sunday 3:00:00 PM - 6:00:00 PM Room: Exhibit HallPurpose: To develop a dynamic model that explains oxygen dynamics between the microvascular perfusion and the hypoxic cell population inside a tumor.
Methods: Bussink et al (Radiat Res 153(4), p.398 (2000)) observed fast oxygen dynamics, faster than cell-death. Based on a simplified three-compartment-model: the microvasculature, well-oxygenated, and hypoxic tumor cell populations. We applied a first-order differential model for the tumor's transient response as a function of oxygen content within the blood vessels. The sink terms in our model for each compartment are fast changing parameters because radiation rapidly changes the oxygen consumption of the tumor cell in a time scale which is much faster than the population changes of the tumor. Transportation balance condition is also applied for each compartment.
Results: Our simulation results can explain the experimental data in Bussink et al's (Radiat Res 153(4), p.398 (2000)) paper. We provide an explanation for the relative complex behavior of the microvascular perfusion after radiation that emphasizes the role of dynamic metabolic changes in addition to population changes.
Conclusions: A newly developed dynamic model leads our understanding to the interrelationship between microvascular oxygen content within the blood vessels and the hypoxia state of the tumor to a deeper level, which has the potential to provide the theoretical foundation for the patient'specific adaptive radiotherapy.
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