POLQ-driven repair scars shape the immunogenic landscape of homologous recombination-deficient pancreatic cancer
This study identifies the POLQ-driven MMEJ Deletion Footprint (MDF) as a key genomic marker in homologous recombination-deficient pancreatic cancer that promotes immunogenicity by increasing neoantigens, remodeling myeloid cells to enhance antigen presentation, and fostering productive T-cell interactions, thereby linking specific DNA repair mechanisms to favorable clinical responses to immunotherapy.