ABSTRACT
Since the early years of radiation therapy it has been appreciated that the biological effect of a given physical absorbed dose of ionizing radiation depends on how this dose is distributed over time. For many years, the differential response of tumours and normal tissues to changes in dose-time fractionation appeared to be the most important means of improving the therapeutic ratio. Mathematical models – often referred to as bioeffect models – were first introduced in the 1920s with the aim of quantifying the biological effect of dose-fractionation schedules on tumour control and normal-tissue side-effects. As discussed in Chapter 8, the linear-quadratic (LQ) model was introduced around 1980 and has gradually become
the model of choice for bioeffect estimation in radiotherapy. In the beginning, the use of the LQ model was conceptually linked to the target-cell hypothesis. However, there is increasing evidence that many late effects, and even some early effects, of radiation therapy are not directly related to simple killing of a defined population of target cells (see Chapter 13, and Bentzen, 2006). The most prevalent current view is that the LQ approach represents an approximate, pragmatic method for converting dose-time fractionation schedules into a biologically effective dose. The LQ model has a limited range of applicability, and extrapolations outside the range of available data should only be performed with the greatest care. Model parameters should be estimated from clinical observations and their statistical precision should be taken into account when used to estimate the biological effect of a given schedule.
