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Adv."],"published-print":{"date-parts":[[2026,10,23]]},"abstract":"<jats:p>\n                    Acute myeloid leukemia (AML) is marked by unchecked expansion of undifferentiated myeloid cells. Although oncogenic fusions such as MLL-AF9 can initiate disease, the early steps of leukemogenesis and the role of cell-intrinsic regulators remain unclear. We previously showed that the Polycomb-associated factor Phf19 is required for hematopoietic stem cell (HSC) maintenance and state control in mice and that its loss (Phf19\n                    <jats:sup>KO<\/jats:sup>\n                    ) impairs HSC function. To define Phf19\u2019s role in transformation, we expressed MLL-AF9 in Phf19\n                    <jats:sup>KO<\/jats:sup>\n                    hematopoietic cells and performed integrated multiomic analyses. Phf19 deletion promoted acquisition of stemlike features and reduced responsiveness to differentiation-inducing AML therapies. Molecular and functional consequences of Phf19 loss paralleled those observed in the datasets of patients with AML. From these data, we derived a prognostic signature\u2014PHFScore\u2014which reveals previously unrecognized AML survival-correlating genes that robustly stratify patients across distinct cellular origins and leukemogenic stages, underscoring Phf19\u2019s key role in AML biology and prognosis.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aed6757","type":"journal-article","created":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T17:58:42Z","timestamp":1792778322000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["Polycomb factor PHF19 affects AML initiation, patient prognosis, and survival"],"prefix":"10.1126","volume":"12","author":[{"given":"Gianni Paolo","family":"Gamarra Figueroa","sequence":"first","affiliation":[{"name":"Centre for Genomic Regulation (CRG), The Barcelona Institute for Science and Technology, Carrer del Doctor Aiguader 88, Barcelona 08003, 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