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Adv."],"published-print":{"date-parts":[[2026,8,14]]},"abstract":"<jats:p>\n                    Acute myeloid leukemia (AML) is an aggressive hematological malignancy arising from hematopoietic stem and progenitor cells (HSPCs). Current treatments often fail to eradicate AML; therefore, new therapeutic strategies are essential. Here, we reveal that RNA terminal uridylyl transferase enzymes 4 and 7 (TUT4\/7) are druggable therapeutic targets, whose genetic deletion suppresses AML growth, induces apoptosis, and improves the survival in leukemic mouse models. Notably, a preclinical TUT4\/7 inhibitor promotes cell death in samples from patients with AML and synergizes with venetoclax. Mechanistically, TUT4\/7 inactivation suppresses mevalonate pathway gene expression, compromising the cholesterol synthesis pathway. Current AML therapies often cause severe hematopoietic toxicity. Although\n                    <jats:italic toggle=\"yes\">Tut4\/7<\/jats:italic>\n                    deletion results in inflammatory activation throughout the hematopoietic system, this is permissive to a normal life span and\n                    <jats:italic toggle=\"yes\">Tut4\/7<\/jats:italic>\n                    deficiency does not compromise HSPC function. Together, these findings identify TUT4\/7 as druggable targets, whose inactivation suppresses AML while sparing normal hematopoiesis. In combination with venetoclax, this represents a promising therapeutic strategy.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aec3399","type":"journal-article","created":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T18:01:07Z","timestamp":1786557667000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["RNA terminal uridylyl transferases are druggable vulnerabilities in AML but are dispensable for normal hematopoiesis"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2059-7006","authenticated-orcid":true,"given":"Christopher","family":"Mapperley","sequence":"first","affiliation":[{"name":"Division of Cancer Biology, The Institute of Cancer Research, London, UK."},{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-9255-4999","authenticated-orcid":true,"given":"Elise","family":"Georges","sequence":"additional","affiliation":[{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-8294-1811","authenticated-orcid":true,"given":"Ali A.","family":"Azar","sequence":"additional","affiliation":[{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."},{"name":"Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK."},{"name":"Division of Genome Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8340-7196","authenticated-orcid":true,"given":"Yuka","family":"Kabayama","sequence":"additional","affiliation":[{"name":"Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK."},{"name":"Institute of Cell Biology, University of Edinburgh, Edinburgh, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-4129-0014","authenticated-orcid":true,"given":"Hannah","family":"Lawson","sequence":"additional","affiliation":[{"name":"Division of Cancer Biology, The Institute of Cancer Research, London, UK."},{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9385-0359","authenticated-orcid":true,"given":"Iwo","family":"Kucinski","sequence":"additional","affiliation":[{"name":"Department of Haematology, Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek","family":"George","sequence":"additional","affiliation":[{"name":"Division of Cancer Biology, The Institute of Cancer Research, London, UK."},{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joana","family":"Campos","sequence":"additional","affiliation":[{"name":"Division of Cancer Biology, The Institute of Cancer Research, London, UK."},{"name":"Barts Cancer Institute, Queen Mary University of London, London, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-6315-1425","authenticated-orcid":true,"given":"Corey","family":"Fyfe","sequence":"additional","affiliation":[{"name":"Redona Therapeutics, Watertown, MA. 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