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Increased proportion of mature NK cells is associated with successful imatinib discontinuation in chronic myeloid leukemia.
Helsingin Yliopisto, Hematology Research Unit Helsinki, Helsinki, Finland.
Akademiska Sjukhuset, Department of Medical Sciences, Uppsala, Sweden.
Karolinska Institutet, Department of Medicine, Stockholm, Sweden.
Centre Hospitalier Universitaire de Poitiers, Poitiers, France.
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2017 (English)In: Leukemia, ISSN 0887-6924, E-ISSN 1476-5551, Vol. 31, no 5, 1108-1116 p.Article in journal (Refereed) Published
Abstract [en]

Recent studies suggest that a proportion of chronic myeloid leukemia (CML) patients in deep molecular remission can discontinue the tyrosine kinase inhibitor (TKI) treatment without disease relapse. In this multi-center, prospective clinical trial (EURO-SKI, NCT01596114) we analyzed the function and phenotype of T and NK cells and their relation to successful TKI cessation. Lymphocyte subclasses were measured from 100 imatinib-treated patients at baseline and 1 month after the discontinuation, and functional characterization of NK and T cells was done from 45 patients. The proportion of NK cells was associated with the molecular relapse-free survival as patients with higher than median NK-cell percentage at the time of drug discontinuation had better probability to stay in remission. Similar association was not found with T or B cells or their subsets. In non-relapsing patients the NK-cell phenotype was mature, whereas patients with more naïve CD56(bright) NK cells had decreased relapse-free survival. In addition, the TNF-α/IFN-γ cytokine secretion by NK cells correlated with the successful drug discontinuation. Our results highlight the role of NK cells in sustaining remission and strengthen the status of CML as an immunogenic tumor warranting novel clinical trials with immunomodulating agents.

Place, publisher, year, edition, pages
Nature Publishing Group, 2017. Vol. 31, no 5, 1108-1116 p.
National Category
Cancer and Oncology Hematology Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:oru:diva-60955DOI: 10.1038/leu.2016.360ISI: 000400464800009PubMedID: 27890936Scopus ID: 2-s2.0-85006312419OAI: oai:DiVA.org:oru-60955DiVA: diva2:1140584
Note

Funding agencies:

Nordic Cancer Union

Finnish Society of Hematology

Biomedicum Helsinki Foundation

Research Foundation of Blood Diseases in Finland

Academy of Finland

Finnish Cancer Organizations

Signe and Ane Gyllenberg Foundation

Finnish Cancer Institute

Doctoral Programme in Clinical Research in the University of Helsinki

Available from: 2017-09-12 Created: 2017-09-12 Last updated: 2017-09-12Bibliographically approved

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