Effects of 5-azacytidine on natural killer cell activating receptor expression in patients with refractory anemia with excess of blasts

• Main Authors: Régis T. Costello, Amélie Leclercq, Thérèse Le Treut, Carole Sanchez, Delphine Mercier, Gérard Sébahoun
• Format: Article
• Language: English
• Published: Elsevier 2015-01-01
• Series: Leukemia Research Reports
• Subjects: Natural killer cells; Refractory anemia with excess of blasts; Natural cytotoxicity receptors; Demethylation; 5-azacytidine
• Online Access: http://www.sciencedirect.com/science/article/pii/S2213048915000023

Epigenetic drugs modify DNA methylation and are used in refractory anemia with excess of blasts (RAEB). These drugs may reactivate anti-oncogene expression and restore a normal phenotype instead of inducing antitumor toxicity, although they also have immunosuppressive effects on T-lymphocytes [1] In RAEB and acute myeloid leukemia, a defect in natural killer (NK) cell cytotoxicity has been shown, which relies on abnormal expression of activating receptors. Previous study has shown that 5-azacytidine impaired mRNA synthesis and induced apoptosis in NK cells [2]. In this study we investigated the effect of the demethylating drug 5-azacytidine (Vidaza®) on NK receptors with the hypothesis that demethylation of the promoters of activating NK receptor genes induces gene reactivation and thus may increase their expression.