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FLASH radiotherapy (FLASH-RT) has shown the potential to spare normal tissuewhile seemingly maintaining the effectiveness of conventional radiotherapy(CONV-RT). It has been suggested that the protective effect arises from theradiolytic oxygen depletion (ROD) caused by FLASH-RT, but it is not entirelyclear why this protective effect is not observed in tumors. Iso-effectivenesshas been experimentally observed in time-volume curves of preclinical tumorsirradiated with FLASH and conventional radiotherapy, but it may not translateto clinical trials, where tumor control probability (TCP) is typically theinvestigated endpoint.  In this work, we used mathematical models to investigate theiso-effectiveness of FLASH-RT/CONV-RT on tumors, focusing on the role of ROD.We used a spatiotemporal reaction-diffusion model, including ROD, to simulatetumor oxygenation. From those oxygen distributions we obtained survivingfractions (SFs), using the linear-quadratic model with oxygen enhancementratios (OER). We then used the calculated SFs to describe the evolution ofpreclinical tumor volumes through a mathematical model of tumor response. Wealso calculated TCPs using the Poisson-LQ approach.  Our study suggests that ROD causes differences in SF between FLASH-RT andCONV-RT, especially in low $\alpha$/$\beta$ and poorly oxygenated cells. Thesechanges do not lead to significant differences in the evolution of preclinicaltumors. However, when extrapolating this effect to TCP curves, we observedimportant differences between both techniques (TCP is lower in FLASH-RT).Nonetheless, it cannot be discarded that other effects not modeled in this workcould contribute to tumor control and maintain the iso-effectiveness ofFLASH-RT.

An in-silico study of conventional and FLASH radiotherapy  iso-effectiveness: Radiolytic oxygen depletion and its potential impact on  tumor control probability