Advances in Molecular OncologyAdvances in Molecular OncologyУспехи молекулярной онкологии2313-805X2413-3787Publishing House ABV Press74710.17650/2313-805X-2025-12-4-51-61REVIEW ARTICLESОБЗОРНЫЕ СТАТЬИReview ArticleAID/APOBEC family and its role in carcinogenesisСемейство AID/APOBEC и его роль в канцерогенезеhttps://orcid.org/0000-0002-6817-2103VolgarevaG. M.ВолгареваГ. М.
Russian Federation
galina.volgareva@ronc.ruN.N. Blokhin National Medical Research Center of Oncology, Ministry of Health of RussiaФГБУ «Национальный медицинский исследовательский центр онкологии им. Н.Н. Блохина» Минздрава России1412202512451611802202521092025Copyright ©; 2025, Volgareva G.M.Copyright ©; 2025, Волгарева Г.М.2025Volgareva G.M.Волгарева Г.М.https://creativecommons.org/licenses/by/4.0https://umo.abvpress.ru/jour/article/view/747

The AID/APOBEC gene family originated during evolution to perform functions related to organismal defense. At present, AID/APOBEC genes encode proteins that are structurally similar but functionally diverse. Most AID/APOBEC proteins exhibit deaminase activity toward cytidyl nucleotides in single-stranded DNA and RNA. In addition to cytidine deamination within viral genomes – which restricts infection – these deaminases are also capable of inducing mutations in the human genome. APOBEC-associated mutations represent one of the most common mutational signatures in cancer: they have been detected in approximately 75 % of cancer types and in more than 50 % of all tumors.

The aim of this review is to analyze the role of AID/APOBEC-induced mutations in the genesis of human malignancies.

Семейство генов AID/APOBEC возникло в ходе эволюции для осуществления функций защиты организма. Современные гены AID/APOBEC кодируют белки, сходные по строению, но значительно различающиеся функционально. Большинство белков AID/APOBEC обладают дезаминазной активностью в отношении цитидиловых нуклеотидов в составе однонитевой ДНК и РНК. Помимо дезаминирования цитозина в составе геномов вирусов, что приводит к ограничению (рестрикции) инфекции, эти цитидиндезаминазы способны вызывать мутации в геноме человека. APOBEC-ассоциированные мутации представляют собой один из наиболее распространенных видов мутаций в злокачественных новообразованиях, они выявлены приблизительно в 75 % типов рака, более чем в 50 % всех новообразований.

Цель обзора – анализ роли мутаций, индуцированных цитидиндезаминазами AID/APOBEC, в генезе злокачественных новообразований человека.

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