An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers.

摘要: Recent studies indicate that a subclass of APOBEC cytidine deaminases, which convert cytosine to uracil during RNA editing and retrovirus or retrotransposon restriction, may induce mutation clusters in human tumors. We show here throughout cancer genomes APOBEC-mediated mutagenesis is pervasive correlates with mRNA levels. Mutation whole-genome exome data sets conformed the stringent criteria indicative an pattern. Applying these 954,247 mutations 2,680 exomes from 14 types, mostly The Cancer Genome Atlas (TCGA), showed significant presence pattern bladder, cervical, breast, head neck, lung cancers, reaching 68% all some samples. Within breast cancer, HER2-enriched subtype was clearly enriched for tumors pattern, suggesting this type functionally linked development. also extended cancer-associated genes, implying ubiquitous carcinogenic.