ArticleMedical physics2026
A modified lethal-potentially lethal model for oxygen-mediated FLASH sparing in stem cell niches.
Article in Medical physics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundUltra-high dose rate (FLASH) irradiation can reduce normal-tissue toxicity while preserving tumor control, but a mechanistic explanation consistent with classical radiobiology remains incomplete. In particular, oxygen-depletion arguments based solely on bulk tissue oxygenation can appear inconsistent with clinically relevant fraction sizes, motivating a DNA-target-level oxygen formulation. PURPOSE: To develop a theory-based mechanistic extension of the Lethal and Potentially Lethal (LPL) model that explains oxygen-mediated FLASH trends without prescribing dose rate-dependent radiosensitivity, and to identify the baseline nuclear oxygen window in which sparing is expected to be largest.
methodsWe introduce an explicit Precursor Lesion population whose fate is governed by competing chemical restitution/repair versus oxygen-dependent fixation into potentially lethal and lethal lesion channels. Fixation kinetics are coupled to a time-varying nuclear oxygen tension,
resultsThe model predicts that oxygen-mediated FLASH sparing is largest when baseline nuclear oxygenation lies in an intermediate physiologic-hypoxia regime, corresponding to the steep oxygen-responsive portion of the OER curve. In the reference parameter set, a quiescent normal-tissue niche with baseline
conclusionsBy explicitly resolving Precursor Lesion fixation kinetics and by treating niche-to-nucleus oxygenation as an effective target-level variable, this mechanistic LPL framework predicts that oxygen-mediated FLASH sparing is most likely when baseline oxygenation lies within an intermediate physiologic-hypoxia window. The model should therefore be viewed as a mechanistic, testable framework rather than as a universal explanation of all FLASH responses.
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