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

Jlenia Guarnerio, Lourdes Maria Mendez, Noboru Asada, Archita Venugopal Menon, Jacqueline Fung, Kelsey Berry, Paul S. Frenette, Keisuke Ito and Pier Paolo Pandolfi ()
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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

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-017-02427-x

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