ABSTRACT
The exact origins and credit for using X-rays therapeutically, as opposed to diagnostically, are shrouded in some mystery and controversy. Quantitative models have been fairly widely used in radiation therapy, and at least three major areas have received significant theoretical attention: the underlying mechanisms for lethality in relation to dose-response curves, the kinetics of radiation-induced damage repair, and optimal fractionation of radiation regimes for various cancers. Many of the more mechanistic lesion-interaction and even saturable repair models of radiation-induced cell death approximate the linear-quadratic model within the clinically relevant range of radiation doses. Acute doses of ionizing radiation rapidly induce double-stranded breaks (DSBs) through free-radical reactions in the nuclear deoxyribonucleic acid (DNA) (chromatin), and such breaks are widely believed to be the principle cause of radiation-induced cell death. Lethal-potentially lethal model includes cytotoxicity from incorrectly repaired and initially irreparable, lethal DSBs.
