If radiotherapy hurts your skin, it’s genetic

A team from Université Paris-Saclay have discovered a gene that makes some cancer patients more sensitive to radiotherapy. The discovery means that medicine could be personalised to save people’s skin and continue treatment they may have stopped due to pain. 

95% of cancer patients undergoing radiation therapy experience radiation damage to the skin around the treatment area called acute dermatitis. The discomfort and pain from dermatitis can force patients to discontinue treatment – with serious consequences.

However, skin damage varies from person to person. A team from the Institute of Cellular and Molecular Radiobiology from CEA, in partnership with Inserm and University Paris-Sud, have discovered that these differences are due to the TRAIL gene that’s involved in the death of cells.

The gene allows a cell to produce a protein. When this protein binds in large quantities with specific receptors, the cell dies. The death of many skin cells causes dermatitis.

In the study published on the Oncotarget website, scientists showed that the TRAIL gene exists in three forms. Two of these forms lead to a high production of TRAIL proteins. Radiation makes the TRAIL protein’s receptors active, so if a patient's cells contain a lot of TRAIL protein at the time they undergo radiotherapy, skin cells die in large quantities and the patient is labelled as ‘radiosensitive’. 

On the other hand, a 'radioresistant’ patient does not produce a lot of TRAIL protein and therefore does not suffer from severe dermatitis.

Post-radiotherapy complications, such as dermatitis, are therefore due to the type of TRAIL gene the patient has. Knowing the type of radiosensitivity a patient is before starting radiotherapy could allow doctors to adjust treatment – in both duration and dose – and save patients’ skin.

Recent Issues