癌症的发生、进展和复发往往由体细胞内发生的突变所导致。因此，提高突变率的过程会加速癌变过程，并阻碍长效治疗的发展。最近对人类癌症基因组的测序已经确定了突变模式，被称为突变签名，其中很多与特定的环境诱导和内源性突变过程相对应。一些最常见的突变签名是由APOBECs活性失调引起的，它们在特定序列基序中对单链DNA中的胞嘧啶进行去氨基化，引起C-T和C-G的替代。在人类中，APOBEC产生的肿瘤细胞遗传异质性促进了癌症的发生、转移和对治疗的抵抗。在这里，我们回顾APOBECs在癌症突变发生中的作用及其对疾病和影响APOBEC突变能力的生物过程的当前认识。

The initiation, progression, and relapse of cancers often result from mutations occurring within somatic cells. Consequently, processes that elevate mutation rates accelerate carcinogenesis and hinder the development of long-lasting therapeutics. Recent sequencing of human cancer genomes has identified patterns of mutations, termed mutation signatures, many of which correspond to specific environmentally induced and endogenous mutation processes. Some of the most frequently observed mutation signatures are caused by dysregulated activity of APOBECs, which deaminate cytidines in single-stranded DNA at specific sequence motifs causing C-to-T and C-to-G substitutions. In humans, APOBEC-generated genetic heterogeneity in tumor cells contributes to carcinogenesis, metastasis, and resistance to therapeutics. Here, we review the current understanding of APOBECs' role in cancer mutagenesis and impact on disease and the biological processes that influence APOBEC mutagenic capacity.