Preclinical investigation uncovers repair mechanisms for APOBEC3A-induced double-strand breaks in urothelial cancer, highlighting polymerase theta synthetic lethality as a targeted strategy.
BackgroundAPOBEC3 cytidine deaminase enzymes are major drivers of cancer evolution, genomic instability, tumor heterogeneity and therapeutic resistance, yet no therapy selectively targets tumors with APOBEC3 activity.We investigated how APOBEC3A-induced double-strand breaks (DSBs) are repaired and whether this creates a therapeutically targetable vulnerability in APOBEC3A-high urothelial tumor.
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Abhishek Bose (2026) studied this question.
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