Mani Larijani

Apr 8, 2024 | cell.com | Aaron N. Hata |Mani Larijani |Simon FRASER

APOBEC3 cytidine deaminases have emerged as key drivers of mutagenesis in a wide spectrum of tumor types and are now appreciated to play a causal role in driving tumor evolution and drug resistance. As efforts to develop APOBEC3 inhibitors progress, understanding the timing and consequences of APOBEC3-mediated mutagenesis in distinct clinical contexts will be critical for guiding the development of anti-cancer therapeutic strategies.

Jun 20, 2023 | frontiersin.org | Nanyang Normal |Matilde E. LLeonart |Mani Larijani |Xiaoxia Liu

1 IntroductionThe human APOBEC3 (apolipoprotein B mRNA editing catalytic polypeptide-like 3, A3s) gene family consists of seven cytidine deaminases (A3A, A3B, A3C, A3D, A3F, A3G, and A3H), which are located on chromosome 22 (1). Members of the A3 family reportedly play a role in the innate immune response to viral infections and can also cause damage to cellular DNA, potentially contributing to the initiation and progression of cancer (2, 3).