Epigenetic therapies for neuroblastoma : immunogenicity awakens

The development of immunotherapies for neuroblastoma remains challenging owing to the low immunogenicity of neuroblastoma cells, as reflected by the low expression of one of the main triggers of immune recognition, the major histocompatibility complex class I (MHC-I). Cornel et al. showed that epigenetic modulation of neuroblastoma cells with a histone deacetylase inhibitor can boost the expression of major histocompatibility complex class I, among other immune receptors, priming their recognition by T- and natural killer cells. By leveraging the developmentally related aberrant epigenetic landscapes of neuroblastoma, these discoveries pave the way to overcome a major limitation in the field of neuroblastoma immunotherapy. Immunotherapies against the aggressive childhood tumour neuroblastoma remain challenged due to its low capacity of response to the immune system action. A recent work shows that that its immune responsiveness can be restored with entinostat, a molecule that promotes an epigenetic modulation that boosts the expression of immunogenic receptors, sensitising neuroblastoma cells to immunotherapy.