Every year, around 2.5 million people in Europe and the United States diagnosed with cancer receive a radiotherapy treatment. However, studies are showing that 30 to 40% of these patients are receiving inefficient treatment due to the radioresistance of their tumour, or are suffering side effects caused by the radiosensitivity of their normal tissues. These numbers highlight the needs of understanding individual radiosensitivity of both the tumour and normal tissues, which might lead to a more personalized treatment.

Recent developments in radiobiology have highlighted the importance of the assessment of radiation-induced DNA double-strand breaks (DSB) repair kinetics in predicting radiosensitivity of both normal and cancerous tissues. In this study, we propose a new mathematical model for healthy tissues based on ATM protein nucleoshuttling, a major actor in DNA DSB repair. Our results were also able to explain the radio-response of a number of genetic syndromes that are known to be radiosensitive.

This model is helping in understanding individual response to ioniring radiation, and can pave the way towards a more complete and predictive model of radiosensitivity and cancer predisposition.