In response to stress or damage, cells undergo senescence and stop dividing. However, if senescent cells accumulate in tissues over the long term, chronic inflammation occurs and the risk of cancer increases. Researchers at the German Cancer Research Center (DKFZ) have now discovered a previously unknown mechanism by which senescent cells protect themselves from oxidative stress and a specific form of cell death known as ferroptosis.
In the long term, these findings could provide new avenues for cancer therapies and the treatment of age-related diseases. The research is published in the journal Cell Death & Differentiation.
Senescence occurs when cells respond to stress or harmful changes and permanently cease their growth. This process is considered a protective mechanism against cancer. For example, cells that carry an oncogene permanently activated by mutations are effectively “frozen” before they can proliferate uncontrollably—a biological emergency program. However, problems arise when senescent cells accumulate in tissue, where they promote chronic inflammation and thus facilitate tumor development. Scientists are therefore searching for ways to eliminate senescent cells before they can cause harm.








