Hundreds of studies in the last decade have established that AID/APOBEC and other DNA-damaging enzymes (e.g. RAG recombinases) can drive and exacerbate cancers. These activities are carried out through mediating genome-wide mutations or double-strand DNA breaks and chromosomal translocations that underlie tumor initiation and drive aggressiveness and treatment resistance during cancer progression. The genome destabilizing activities of these DNA/RNA-damaging enzymes is thus thought to contribute to clonal heterogeneity and evolution of tumors, leading to the current understanding that enzymes that damage DNA/RNA are tumorigenic or pro-tumor. At the same time, emerging hints in the literature point to instances where DNA/RNA-damaging enzyme expression also correlates with anti-tumor phenotypes. Manipulating the activities of these enzymes can afford therapeutic opportunities. Our work in this area includes gaining a better understanding of cellular processes that act up-or downstream from DNA/RNA-editing enzymes and testing the impact of targeted therapies in cancer biology and in immune response to cancer cells. We also work on development of targeted therapeutics.
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