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Significance Somatic mutagenesis is fundamental to the development and evolution of cancers. APOBEC3B (A3B) is a cellular deaminase, which is overexpressed in cancers and believed to be an important cause of cancer-associated mutations. The factors responsible forA3B up-regulation are unknown. Interestingly, a germ-line deletion polymorphism exists, such that a significant proportion of the global population does not express A3B protein. Using large human cancer datasets, we show thatA3B expression is strongly associated with cellular proliferation. Furthermore, we identify a pattern of immune activation related to hypermutation in tumors arising inA3B deletion carriers suggesting that these patients could respond differently to immune-directed therapies. These results provide important context for the ongoing study of A3B as a therapeutic target or biomarker.

APOBEC3B expression in breast cancer reflects cellular proliferation, while a deletion polymorphism is associated with immune activation