{"entity": "researcher", "timestamp": "2026-08-23T09:26:16.740Z", "family": "Dur\u00e1n", "given": "Eduardo", "initials": "E", "orcid": "0000-0001-6974-7004", "affiliations": ["Subdepartamento de Gen\u00f3mica y Gen\u00e9tica Molecular, Secci\u00f3n Gen\u00e9tica Humana, Instituto de Salud P\u00fablica de Chile, Avenida Marathon 1000, \u00d1u\u00f1oa, Santiago 7780050, Chile."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/d04f5bba6fbd4218b6103fb1edc89834.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/d04f5bba6fbd4218b6103fb1edc89834"}}, "publications": [{"entity": "publication", "iuid": "8248b800a72d4fd8ba9f89eb2bd10aac", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8248b800a72d4fd8ba9f89eb2bd10aac.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8248b800a72d4fd8ba9f89eb2bd10aac"}}, "title": "ADAR-Mediated A>I(G) RNA Editing in the Genotoxic Drug Response of Breast Cancer.", "authors": [{"family": "Bernal", "given": "Yanara A", "initials": "YA", "orcid": "0000-0001-9568-0675", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7bde495b5b3e45598324897a86d4cc81.json"}}, {"family": "Dur\u00e1n", "given": "Eduardo", "initials": "E", "orcid": "0000-0001-6974-7004", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d04f5bba6fbd4218b6103fb1edc89834.json"}}, {"family": "Solar", "given": "Isidora", "initials": "I"}, {"family": "Sagredo", "given": "Eduardo A", "initials": "EA", "orcid": "0000-0001-9984-2985", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/76bc874436644ebe8276f29414866635.json"}}, {"family": "Armis\u00e9n", "given": "Ricardo", "initials": "R", "orcid": "0000-0003-2567-0521", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a79c619cae364e38afe9147db691be53.json"}}], "type": "journal article", "published": "2024-07-06", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "25", "issue": "13", "issn-l": null}, "abstract": "Epitranscriptomics is a field that delves into post-transcriptional changes. Among these modifications, the conversion of adenosine to inosine, traduced as guanosine (A>I(G)), is one of the known RNA-editing mechanisms, catalyzed by ADARs. This type of RNA editing is the most common type of editing in mammals and contributes to biological diversity. Disruption in the A>I(G) RNA-editing balance has been linked to diseases, including several types of cancer. Drug resistance in patients with cancer represents a significant public health concern, contributing to increased mortality rates resulting from therapy non-responsiveness and disease progression, representing the greatest challenge for researchers in this field. The A>I(G) RNA editing is involved in several mechanisms over the immunotherapy and genotoxic drug response and drug resistance. This review investigates the relationship between ADAR1 and specific A>I(G) RNA-edited sites, focusing particularly on breast cancer, and the impact of these sites on DNA damage repair and the immune response over anti-cancer therapy. We address the underlying mechanisms, bioinformatics, and in vitro strategies for the identification and validation of A>I(G) RNA-edited sites. We gathered databases related to A>I(G) RNA editing and cancer and discussed the potential clinical and research implications of understanding A>I(G) RNA-editing patterns. Understanding the intricate role of ADAR1-mediated A>I(G) RNA editing in breast cancer holds significant promise for the development of personalized treatment approaches tailored to individual patients' A>I(G) RNA-editing profiles.", "doi": "10.3390/ijms25137424", "pmid": "39000531", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11242177"}, {"db": "pii", "key": "ijms25137424"}], "notes": [], "created": "2026-08-21T13:03:55.436Z", "modified": "2026-08-21T13:03:55.545Z"}]}