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Peer-reviewedCC BY-NCScience Advances

Polycomb factor PHF19 affects AML initiation, patient prognosis, and survival

  • Gianni Paolo Gamarra Figueroa1
  • Arantxa Gutierrez1
  • Enrique Blanco1
  • Pedro Vizán1,2
  • Cecilia Ballaré1
  • Aleksandra Sparavier1,3
  • Marta Tosto1
  • Saverio Minucci4,5
  • Lars Velten1,6
  • Luciano Di Croce1,6,7
7 affiliations
  1. 1Centre for Genomic Regulation (CRG), The Barcelona Institute for Science and Technology, Carrer del Doctor Aiguader 88, Barcelona 08003, Spain.
  2. 2Universitat Ramon Llull, Blanquerna School of Health Science, Barcelona 08025, Spain.
  3. 3Centre Nacional d’Anàlisi Genòmica (CNAG), Baldiri I Reixac 4, Barcelona 08028, Spain.
  4. 4Department of Experimental Oncology, IEO European Institute of Oncology IRCSS, Milan 20139, Italy.
  5. 5Department of Oncology and Hematology-Oncology, University of Milan, Milan 20122, Italy.
  6. 6Universitat Pompeu Fabra (UPF), Barcelona, Spain.
  7. 7ICREA, Passeig Lluís Companys 23, Barcelona 08010, Spain.
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Abstract

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 (Phf19KO) impairs HSC function. To define Phf19's role in transformation, we expressed MLL-AF9 in Phf19KO 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-PHFScore-which reveals previously unrecognized AML survival-correlating genes that robustly stratify patients across distinct cellular origins and leukemogenic stages, underscoring Phf19's key role in AML biology and prognosis.

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Cite

BibTeXRIS
BibTeX
@article{figueroa2026polycomb,
  title = {{Polycomb factor PHF19 affects AML initiation, patient prognosis, and survival}},
  author = {Gianni Paolo Gamarra Figueroa and Arantxa Gutierrez and Enrique Blanco and Pedro Vizán and Cecilia Ballaré and Aleksandra Sparavier and Marta Tosto and Saverio Minucci and Lars Velten and Luciano Di Croce},
  journal = {Science Advances},
  year = {2026},
  month = oct,
  doi = {10.1126/sciadv.aed6757},
  url = {https://www.science.org/doi/10.1126/sciadv.aed6757},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Polycomb factor PHF19 affects AML initiation, patient prognosis, and survival
AU  - Gianni Paolo Gamarra Figueroa
AU  - Arantxa Gutierrez
AU  - Enrique Blanco
AU  - Pedro Vizán
AU  - Cecilia Ballaré
AU  - Aleksandra Sparavier
AU  - Marta Tosto
AU  - Saverio Minucci
AU  - Lars Velten
AU  - Luciano Di Croce
PY  - 2026
DA  - 2026/10/23
JO  - Science Advances
DO  - 10.1126/sciadv.aed6757
UR  - https://www.science.org/doi/10.1126/sciadv.aed6757
AB  - 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 (Phf19KO) impairs HSC function. To define Phf19's role in transformation, we expressed MLL-AF9 in Phf19KO 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-PHFScore-which reveals previously unrecognized AML survival-correlating genes that robustly stratify patients across distinct cellular origins and leukemogenic stages, underscoring Phf19's key role in AML biology and prognosis.
SN  - 2375-2548
ER  -