Pharmacologic Modification of Radiation-Induced Late Normal Tissue Injury

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Abstract

Classically, late radiation-induced normal tissue morbidity has been viewed as due solely to a delayed reduction in the number of surviving clonogens of either parenchymal [1] or vascular [2] target cell populations. These chronic late effects have been held to be inevitable, progressive, and untreatable [2]. In the classical model, the progressive and untreatable nature of late tissue damage follows from the assumption that the decline in clonogen number is due to mitotic cell death that results from genetic injury produced at the time of irradiation and irrevocably fixed in place within hours after irradiation. The long latent period for the expression of injury in tissues such as the kidney, lung, and spinal cord is explained by assuming that the target clonogenic cell population has a very long doubling time.