On January 7, 2025, researchers at the University of California, Irvine, announced a significant discovery regarding the mechanisms of DNA damage response in cells. This research could lead to advancements in personalized cancer treatments.
The study, published in Nature Structural & Molecular Biology, identifies a new pathway that activates the protein NF-κB, which plays a crucial role in the body's inflammatory response to DNA damage. The research team, led by postdoctoral fellow Elodie Bournique, found that the enzyme IRAK1 becomes activated in response to DNA damage caused by UV exposure or certain chemotherapy drugs, differing from the previously known ATM enzyme.
The researchers observed that damaged cells release the protein IL-1α, which signals neighboring cells to activate IRAK1, initiating the NF-κB inflammatory response. This discovery suggests that the levels of IL-1α and IRAK1 vary across different cancer cell types, indicating that cancer treatments may need to be tailored to individual patient profiles.
Dr. Rémi Buisson, the study's lead author, emphasized the potential for these findings to improve treatment efficacy and reduce side effects by personalizing therapies based on specific cancer cell responses. The research team plans to continue their investigations using mouse models to further explore this newly identified pathway.