Philadelphia-negative myeloproliferative neoplasms as disorders marked by cytokine modulation

Cytokines are key immune mediators in physiological and disease processes, whose increased levels have been associated with the physiopathology of hematopoietic malignancies, such as myeloproliferative neoplasms. This study examined the plasma cytokine profiles of patients with essential thrombocyth...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Hematology, Transfusion and Cell Therapy Transfusion and Cell Therapy, 2018-04, Vol.40 (2), p.120-131
Hauptverfasser: Cacemiro, Maira da Costa, Cominal, Juçara Gastaldi, Tognon, Raquel, Nunes, Natalia de Souza, Simões, Belinda Pinto, Figueiredo-Pontes, Lorena Lôbo de, Catto, Luiz Fernando Bazzo, Traina, Fabíola, Souto, Elizabeth Xisto, Zambuzi, Fabiana Albani, Frantz, Fabiani Gai, Castro, Fabíola Attié de
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Cytokines are key immune mediators in physiological and disease processes, whose increased levels have been associated with the physiopathology of hematopoietic malignancies, such as myeloproliferative neoplasms. This study examined the plasma cytokine profiles of patients with essential thrombocythemia, primary myelofibrosis, polycythemia vera and of healthy subjects, and analyzed correlations with JAK2 V617F status and clinical-hematological parameters. The proinflammatory cytokine levels were increased in myeloproliferative neoplasm patients, and the presence of the JAK2 V617F mutation was associated with high IP-10 levels in primary myelofibrosis patients. Essential thrombocythemia, primary myelofibrosis, and polycythemia vera patients exhibited different patterns of cytokine production, as revealed by cytokine network correlations. Together, these findings suggest that augmented cytokine levels are associated with the physiopathology of myeloproliferative neoplasms.
ISSN:2531-1379
2531-1387
2531-1387
DOI:10.1016/j.htct.2017.12.003