突变
胞苷
癌症
阿波贝克
抗药性
癌症研究
生物
突变
计算生物学
遗传学
基因
基因组
酶
生物化学
作者
Aaron N. Hata,Mani Larijani
出处
期刊:Cancer Cell
[Elsevier]
日期:2024-04-01
卷期号:42 (4): 497-501
被引量:3
标识
DOI:10.1016/j.ccell.2024.03.010
摘要
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. 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.
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