The APOBEC family of cytidine deaminases has been proposed to represent a major enzymatic source of mutations in cancer. Here, we summarize available evidence that links APOBEC deaminases to cancer mutagenesis. We also highlight newly identified human cell models of APOBEC mutagenesis, including cancer cell lines with suspected endogenous APOBEC activity and a cell system of telomere crisis-associated mutations. Finally, we draw on recent data to propose potential causes of APOBEC misregulation in cancer, including the instigating factors, the relevant mutator(s), and the mechanisms underlying generation of the genome-dispersed and clustered APOBEC-induced mutations.

APOBEC 胞苷脱氨酶家族被认为是癌症突变的主要酶源。在这里，我们总结了将 APOBEC 脱氨酶与癌症突变联系起来的现有证据。我们还重点介绍了新发现的 APOBEC 突变人类细胞模型，包括疑似具有内源性 APOBEC 活性的癌细胞系和端粒危机相关突变的细胞系统。最后，我们利用最近的数据提出了癌症中 APOBEC 失调的潜在原因，包括诱发因素、相关突变因子以及基因组分散和聚集的 APOBEC 诱导突变的产生机制。