Research: Upregulation of APOBECs have been documented in many cancers, where it acts to mutate cytosine to uracil. These mutations have led to a unique signature dominated by C-to-T, C-to-G, and C-to-A transitions. Within this deaminase family of enzymes, APOBEC3B (A3B) has been demonstrated to have increased expression levels in breast cancer. A3B is unique among the larger APOBEC family for its nuclear localization. As a result, A3B has direct access to endogenous DNA, giving it a greater opportunity to act as a driver of tumor formation. This increased level has been known to cause tumor heterogeneity and drug resistance in animal models. It remains to be identified how A3B affects the development of treatment resistance and for which treatments. My work aims to determine whether A3B alters treatment outcomes for patients with breast cancer and if so, determine the mechanism by which this might be occurring.
