A cancer drug target already being investigated in clinical trials turns out to be doing something even more consequential than researchers realized. Scientists at Scripps Research have discovered that the enzyme Pol theta (Polθ) drives a DNA repair mechanism directly at broken replication forks—one of the most frequent forms of DNA damage in cancer cells. The findings, published in Molecular Cell on March 16, 2026, help explain how tumors survive relentless replication stress and clarify why Pol theta inhibitors may be an effective strategy to selectively target cancer.
This article was originally published on MedicalXpress.com
