Abstract
The radiation killing of tumor cells by ionizing radiation is best described by the linear–quadratic (LQ) model. Research into the underlying mechanisms of α- and β-inactivation has suggested that different molecular targets (DNA in different forms) and different microdosimetric energy deposits (spurs versus electron track-ends) are involved. Clinical protocols with fractionated doses of about 2.0 Gy/day were defined empirically, and we now know that they produce cancer cures mainly by the α-inactivation mechanism. Radiobiology studies indicate that α and β mechanisms exhibit widely different characteristics that should be addressed upfront as clinical fractionation schemes are altered. As radiation treatments attempt to exploit the advantages of larger dose fractions over shorter treatment times, the LQ model can be used to predict iso-effective tumor cell killing and possibly iso-effective normal tissue complications. Linking best estimates of radiobiology and tumor biology parameters with tumor control probability (TCP) and normal tissue complication probability (NTCP) models will enable us to improve and optimize cancer treatment protocols, delivering no more fractions than are strictly necessary for a high therapeutic ratio.
Highlights
A linear–quadratic (LQ) relationship precisely describes the radiation killing of human tumor cells when important experimental factors are controlled [1]
The most important are the use of cell populations of homogeneous radiosensitivity and the minimization of sublesion damage repair during radiation exposures
We recommend that α and βo be used only to describe the inactivation rates of homogeneous cell populations irradiated in this manner [5]
Summary
A linear–quadratic (LQ) relationship precisely describes the radiation killing of human tumor cells when important experimental factors are controlled [1]. It is likely that this value of √βo is lower than 0.241 Gy−1 (the average in Table 1) since most of the studies were performed at room temperature or at 37°C, where some repair of the sublesions of β-killing would be expected during radiation exposures.
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