Cancer’s “Undruggable” Protein Has a Dangerous New Superpower

Scientists at Oregon Health & Science University (OHSU) have uncovered a new role for the MYC protein in cancer survival. MYC, which is overactive in most human cancers and drives tumor growth, also helps repair DNA breaks caused by chemotherapy or rapid cell division. This function allows cancer cells to recover from treatment-induced damage, making tumors resistant to therapies designed to destroy them. The study, published in *Genes & Development*, found that MYC physically travels to damaged DNA sites and recruits repair machinery. Senior author Rosalie Sears, Ph.D., explained that MYC’s involvement in DNA repair is nontraditional, as it typically regulates gene activity rather than directly aiding repair processes. Researchers observed that pancreatic cancer cells, which often exhibit high MYC activity, were particularly adept at repairing DNA damage. This ability correlates with poorer patient outcomes, as tumors with active MYC survive chemotherapy and radiation more effectively. First author Gabriel Cohn, Ph.D., noted that MYC helps aggressive cancers like pancreatic cancer tolerate extreme stress from treatment. The findings suggest a potential new treatment strategy: targeting MYC’s DNA repair function to make tumors more susceptible to existing therapies. By blocking this mechanism, scientists may improve the effectiveness of chemotherapy and radiation in cancers where MYC is overactive.