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A non-cell-autonomous role for Pml in the maintenance of leukemia from the niche

Author

Listed:
  • Jlenia Guarnerio

    (Harvard Medical School)

  • Lourdes Maria Mendez

    (Harvard Medical School)

  • Noboru Asada

    (Michael F. Price Center)

  • Archita Venugopal Menon

    (Harvard Medical School)

  • Jacqueline Fung

    (Harvard Medical School)

  • Kelsey Berry

    (Harvard Medical School)

  • Paul S. Frenette

    (Michael F. Price Center)

  • Keisuke Ito

    (Michael F. Price Center)

  • Pier Paolo Pandolfi

    (Harvard Medical School)

Abstract

Disease recurrence after therapy, due to the persistence of resistant leukemic cells, represents a fundamental problem in the treatment of leukemia. Elucidating the mechanisms responsible for the maintenance of leukemic cells, before and after treatment, is therefore critical to identify curative modalities. It has become increasingly clear that cell-autonomous mechanisms are not solely responsible for leukemia maintenance. Here, we report a role for Pml in mesenchymal stem cells (MSCs) in supporting leukemic cells of both CML and AML. Mechanistically, we show that Pml regulates pro-inflammatory cytokines within MSCs, and that this function is critical in sustaining CML-KLS and AML ckit+ leukemic cells non-cell autonomously.

Suggested Citation

  • Jlenia Guarnerio & Lourdes Maria Mendez & Noboru Asada & Archita Venugopal Menon & Jacqueline Fung & Kelsey Berry & Paul S. Frenette & Keisuke Ito & Pier Paolo Pandolfi, 2018. "A non-cell-autonomous role for Pml in the maintenance of leukemia from the niche," Nature Communications, Nature, vol. 9(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02427-x
    DOI: 10.1038/s41467-017-02427-x
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    Cited by:

    1. Sarah Tessier & Omar Ferhi & Marie-Claude Geoffroy & Román González-Prieto & Antoine Canat & Samuel Quentin & Marika Pla & Michiko Niwa-Kawakita & Pierre Bercier & Domitille Rérolle & Marilyn Tirard &, 2022. "Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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