  Radiotherapy is a commonly used treatment for cancer and is usually given in
varying doses. At low radiation doses relatively few cells die as a direct
response to radiation but secondary radiation effects such as DNA mutation or
bystander effects affect many cells. Consequently it is at low radiation levels
where an understanding of bystander effects is essential in designing novel
therapies with superior clinical outcomes. In this article, we use a hybrid
multiscale mathematical model to study the direct effects of radiation as well
as radiation-induced bystander effects on both tumour cells and normal cells.
We show that bystander responses may play a major role in mediating radiation
damage to cells at low-doses of radiotherapy, doing more damage than that due
to direct radiation. The survival curves derived from our computational
simulations showed an area of hyper-radiosensitivity at low-doses that are not
obtained using a traditional radiobiological model.
