Booby Trap: Cancer Gene Spurs Production of DNA-Assaulting Chemicals That Alert and Defuse Rescue Molecule

The study revealed that the activation of the c-myc oncogene in normal human fibroblasts led to significant DNA damage, particularly double-stranded breaks, by increasing the production of reactive oxygen species (ROS). This increase in ROS was shown to damage DNA and activate the p53 protein, which typically halts cell division. However, c-Myc was also found to override p53's function, allowing continued cell proliferation even after DNA damage. The addition of the antioxidant N-acetyl-l-cysteine significantly reduced ROS levels and DNA damage, suggesting that oncogene-induced ROS contribute to genomic instability and cancer development. This research provided new insights into how oncogenes like c-Myc can promote cancer by generating ROS and compromising p53 function, linking genome instability to aging and age-related cancer risk.