Pol is a functional dependency and therapeutic vulnerability in DNMT3A deficient leukemia cells
Bac Viet Le, Umeshkumar M. Vekariya, Monika Maria Toma, Margaret Nieborowska-Skorska, Marie‐Christine Caron, Malgorzata Gozdecka, Zayd Haydar, Martin Walsh, Jayashri Ghosh, Elaine Vaughan‐Williams, Paulina Podszywalow‐Bartnicka, Anna-Mariya Kukuyan, Sylwia Ziółkowska, Jessica Atkins, Emir Hadzijusufovic, , Tomasz Skórski
This study identifies Polθ as a therapeutic target in DNMT3A-mutated leukemia by showing its essential role in DNA repair and replication fork restart, and demonstrates that its inhibition enhances standard therapies.
Cell Reports Medicine · Mar 1, 2026Peer-reviewedCancer Biology