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With great interest we read the recent paper in Mediators of Inflammation by Thomas Stübig and colleagues [1] as the aim of this study was similar to the aim of a study we recently conducted [2], namely, to study the impact of the demethylating agent 5-Azacytidine on the immune system. The two studies, however, reached different conclusions, which as we will discuss below may originate from differences in the patient cohorts and the translation of data from in vitro analyses into in vivo effect. Thus, with the present commentary we would like to discuss the challenges in understanding the true effect of 5-Azacitidine on immune reactivity in cancer patients and how this may depend on the patient group analyzed. 5-Azacytidine was marketed (as Vidaza, Celgene Corporation, Boudry, Switzerland) after a phase III trial revealed it as the first drug prolonging overall survival in high-risk myelodysplastic syndrome (MDS) patients [3]. 5-Azacytidine is known to upregulate the expression of tumor suppressor genes [4], and it has been speculated to what extent it impacts the immune system, both directly and indirectly.

Comment on “5-Azacytidine Promotes an Inhibitory T-Cell Phenotype and Impairs Immune Mediated Antileukemic Activity”