Researchers from LMU University Hospital and the German Cancer Research Center (DKFZ) have identified the protein Dickkopf 3 (DKK3) as a main contributor to long-term skin damage caused by radiotherapy. This discovery could open new avenues for targeted therapies that address chronic inflammation and fibrosis, common side effects of cancer radiation treatment.
Radiotherapy is a widely used method in cancer care, but it often results in lasting skin problems such as thickening, pain, and sensitivity. Currently, these symptoms can only be managed symptomatically and may persist for months or even years after treatment.
The team led by Professor Peter Nelson at LMU University Hospital, along with Roger Sandhoff and Peter E. Huber from DKFZ, found that DKK3 becomes active after radiotherapy within specific skin cells responsible for renewal. This activation sets off processes that promote inflammation and the formation of scar-like tissue, ultimately resulting in chronic skin issues. The work of LMU students Li Li and Khuram Shehzad was instrumental in identifying DKK3’s role and establishing how it functions at a molecular level.
"Drugs that block DKK3 could one day help prevent or reduce long-term skin damage after radiotherapy and thus improve the quality of life of cancer patients and survivors," said Nelson. Researchers are also exploring whether blocking DKK3 might prevent scar formation in other organs.
