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Cited by 63

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Linking the KIR phenotype with STAT3 and TET2 mutations to identify chronic lymphoproliferative disorders of NK cells

Pastoret, Cédric, Desmots, Fabienne, Drillet, Gaëlle, Le Gallou, Simon, Boulland, Marie-Laure, Thannberger, Alexia, Doncker, Anne-Violaine, Salaun, Véronique, Damaj, Gandhi Laurent, Veyrat-Masson, Richard, Tournilhac, Olivier, Moignet, Aline, Pangault, Céline, Roussel, Mikaël, Fest, Thierry, Lamy, Thierry·2021·Blood
DOI 10.1182/blood.2020006721
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Abstract

Distinguishing chronic lymphoproliferative disorders of NK cells (CLPD-NK) from reactive NK-cell expansion is challenging. We assessed the value of killer immunoglobulin-like receptor(KIR) phenotyping and targeted high-throughput sequencing in a cohort of 114 consecutive patients with NK cell proliferation, retrospectively assigned to a CLPD-NK group (n = 46) and a reactive NK group (n = 68). We then developed an NK-cell clonality score combining flow cytometry and molecular profiling with a positive predictive value of 93%. STAT3 and TET2 mutations were respectively identified in 27% and 34% of the patients with CLPD-NK, constituting a new diagnostic hallmark for this disease. TET2-mutated CLPD-NK preferentially exhibited a CD16low phenotype, more frequently displayed a lower platelet count, and was associated with other hematologic malignancies such as myelodysplasia. To explore the mutational clonal hierarchy of CLPD-NK, we performed whole-exome sequencing of sorted, myeloid, T, and NK cells and found that TET2 mutations were shared by myeloid and NK cells in 3 of 4 cases. Thus, we hypothesized that TET2 alterations occur in early hematopoietic progenitors which could explain a potential link between CLPD-NK and myeloid malignancies. Finally, we analyzed the transcriptome by RNA sequencing of 7 CLPD-NK and evidenced 2 groups of patients. The first group displayed STAT3 mutations or SOCS3 methylation and overexpressed STAT3 target genes. The second group, including 2 TET2-mutated cases, significantly underexpressed genes known to be downregulated in angioimmunoblastic T-cell lymphoma. Our results provide new insights into the pathogenesis of NK-cell proliferative disorders and, potentially, new therapeutic opportunities.

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Metadata

Authors
Pastoret, C., Desmots, F., Drillet, G., Le Gallou, S., Boulland, M.-L., Thannberger, A., Doncker, A.-V., Salaun, V., Damaj, G. L., Veyrat-Masson, R., Tournilhac, O., Moignet, A., Pangault, C., Roussel, M., Fest, T., & Lamy, T.
Affiliations
  • Laboratoire d’Hématologie, Centre Hospitalier Universitaire de Rennes, Rennes, France;
  • Service d’Hématologie Clinique, Centre Hospitalier Universitaire (CHU) de Rennes, Rennes, France;
  • Service d’Hématologie Clinique, Hôpital de Saint Malo, Saint Malo, France;
  • Hôpital Privé Sévigné, Cesson-Sévigné, France;
  • Laboratoire d’Hématologie and
  • Service d’Hématologie Clinique, CHU de Caen Normandie, Caen, France;
  • Service d’Hématologie Clinique, CHU de Clermont-Ferrand, Clermont-Ferrand, France; and
  • INSERM, Unité Mixte de Recherche (UMR) 1236, Etablissement Français du sang Bretagne, Université Rennes 1, Rennes, France;
ORCID
Venue
Blood
Publisher
American Society of Hematology
Published
2021-01-15
Volume
137
Issue
23
Pages
3237-3250
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood.2020006721
Cited by
63
References
51
Language
en

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