Abstract

Members of the APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) family of deaminases have been identified as potent mutagens in squamous cell carcinoma arising across all body sites. Previous work has shown that tissue damage-driven squamous cell carcinoma (SCC) arising in the skin of patients with the rare blistering genodermatoses recessive dystrophic epidermolysis bullosa (RDEB) are dominated by APOBEC-driven mutations as well as high mRNA levels of APOBEC3A. Current literature reports APOBEC3B (A3B) and not APOBEC3A (A3A) is capable of localizing to the nucleus of mammalian cells resulting in the notion that A3B and not A3A generates somatic mutations in SCC.

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