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The efficacy of radiotherapy (RT) can be significantly enhanced bycombination with hyperthermia (HT), offering improved therapeutic outcomes atreduced radiation doses. Recent technological advancements have revitalized HTas a promising option for combinatorial RT. However, the underlying mechanisms,implications, and cause-effect relationships require further elucidation forprecise integration into clinical practice. In this context, mathematicalmodeling provides the necessary predicting power for treatment planning.Moreover, based on physicochemical principles, such models help elucidate thebehavior of biological systems under heat. Some cell cultures exhibitdose-dependent changes in therapy response and survival, prompting thedevelopment of a model incorporating cell recovery mechanisms. We extendedJung's model of cellular inactivation by heat based on the accumulation ofsublethal damage to combinatorial radiotherapy in general and incorporateddose-dependent recovery rates. The resulting unified model (Umodel) is suitedto describe (i) individual or sequential treatment/fraction outcomes, (ii)differences and changes in cellular response and recovery or adaptation totreatment, and (iii) the observed sensitivity to treatment order. Wedemonstrate excellent performance (R2 > 0.95) on various cell survival datafrom the literature and our own experimental series. Our observations suggestthat the induction of sublethal damage in cells is pivotal, promoting cellularvulnerability for synergistic outcomes in combined therapeutic schemes.

Generalized mathematical model for adaptive cell survival after thermoradiotherapy: The impact of sublethal damage