Acquired drug resistance to anticancer targeted therapies remains an unsolved clinical
problem. Although many drivers of acquired drug resistance have been identified,,–, the�…

In this study, the impact of the apolipoprotein B mRNA-editing catalytic subunit-like
(APOBEC) enzyme APOBEC3B (A3B) on epidermal growth factor receptor (EGFR)-driven�…

Mutational signatures associated with apolipoprotein B mRNA-editing enzyme catalytic
polypeptide-like (APOBEC) 3 cytosine deaminase activity have been found in over half of�…

The APOBEC3 family of cytosine deaminases has been implicated in some of the most
prevalent mutational signatures in cancer,–. However, a causal link between endogenous�…

Deep sequencing technologies are revealing the complexities of cancer evolution, casting
light on mutational processes fueling tumor adaptation, immune escape, and treatment�…

High rates of APOBEC-signature mutations are found in many tumors, but factors affecting
this mutation pattern are not well understood. Here we explored the contribution of two�…

Breast tumors often display extreme genetic heterogeneity characterized by hundreds of
gross chromosomal aberrations and tens of thousands of somatic mutations. Tumor�…

Recent evidence has implicated APOBEC3B as a source of mutations in cervical, bladder,
lung, head and neck, and breast cancers. APOBEC enzymes normally function in innate�…

The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like APOBEC3A and
APOBEC3B have emerged as key mutation drivers in cancer. Here, we show that�…

APOBEC3B, an anti-viral cytidine deaminase which induces DNA mutations, has been
implicated as a mediator of cancer evolution and therapeutic resistance. Mutational plasticity�…