{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cornel AM"],"funding":["NCI NIH HHS","Villa Joep Foundation"],"pagination":["e005002"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9756225"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(12)"],"pubmed_abstract":["Background
Immunotherapy in high-risk neuroblastoma (HR-NBL) does not live up to its full potential due to inadequate (adaptive) immune engagement caused by the extensive immunomodulatory capacity of HR-NBL. We aimed to tackle one of the most notable immunomodulatory processes in neuroblastoma (NBL), absence of major histocompatibility complex class I (MHC-I) surface expression, a process greatly limiting cytotoxic T cell engagement. We and others have previously shown that MHC-I expression can be induced by cytokine-driven immune modulation. Here, we aimed to identify tolerable pharmacological repurposing strategies to upregulate MHC-I expression and therewith enhance T cell immunogenicity in NBL.Methods
Drug repurposing libraries were screened to identify compounds enhanc"],"journal":["Journal for immunotherapy of cancer"],"pubmed_title":["Epigenetic modulation of neuroblastoma enhances T cell and NK cell immunogenicity by inducing a tumor-cell lineage switch."],"pmcid":["PMC9756225"],"funding_grant_id":["R01 CA271605","IWOV-Actief.51381.180034"],"pubmed_authors":["Essing AHW","Hofman DA","Das S","Szanto CS","van den Beemt DAMH","Lo Presti V","van den Ham F","van Heesch S","Strijker JGM","Wienke J","Nierkens S","Dunnebach E","George RE","Engels SAG","Koopmans B","Molenaar JJ","Dierselhuis MP","Cornel AM","Sengupta S"],"additional_accession":[]},"is_claimable":false,"name":"Epigenetic modulation of neuroblastoma enhances T cell and NK cell immunogenicity by inducing a tumor-cell lineage switch.","description":"Background
Immunotherapy in high-risk neuroblastoma (HR-NBL) does not live up to its full potential due to inadequate (adaptive) immune engagement caused by the extensive immunomodulatory capacity of HR-NBL. We aimed to tackle one of the most notable immunomodulatory processes in neuroblastoma (NBL), absence of major histocompatibility complex class I (MHC-I) surface expression, a process greatly limiting cytotoxic T cell engagement. We and others have previously shown that MHC-I expression can be induced by cytokine-driven immune modulation. Here, we aimed to identify tolerable pharmacological repurposing strategies to upregulate MHC-I expression and therewith enhance T cell immunogenicity in NBL.Methods
Drug repurposing libraries were screened to identify compounds enhanc","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2026-06-15T06:04:08.551Z","creation":"2024-11-13T10:37:59.225Z"},"accession":"S-EPMC9756225","cross_references":{"pubmed":["36521927"],"doi":["10.1136/jitc-2022-005002"]}}