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Nat Commun. 2018 Jan 4;9(1):66. doi: 10.1038/s41467-017-02427-x.

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

Author information

1
Cancer Research Institute, Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA.
2
Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Department of Medicine and Cell Biology, Albert Einstein College of Medicine, Michael F. Price Center, 1301 Morris Park Avenue, Bronx, NY, 10461, USA.
3
Cancer Research Institute, Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA. ppandolf@bidmc.harvard.edu.

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.

PMID:
29302031
PMCID:
PMC5754357
DOI:
10.1038/s41467-017-02427-x
[Indexed for MEDLINE]
Free PMC Article

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