{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Marquardt V"],"funding":["Bundesministerium für Bildung und Forschung","Andrew McDonough B+ Foundation","Deutsche Krebshilfe","Morgan Adams Foundation","German Academic Scholarship Foundation","American Cancer Society-IRG","Wegener Foundation","Deutschen Konsortium für Translationale Krebsforschung","Cancer League of Colorado","Comprehensive Cancer Center Düsseldorf","National Cancer Institute","NCI NIH HHS","Plachy-Rubin Foundation","Hempel Fonden","V Foundation for Cancer Research","NIH HHS","The Broncos Foundation"],"pagination":["e005871"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9843227"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["<h4>Background</h4>While major advances have been made in improving the quality of life and survival of children with most forms of medulloblastoma (MB), those with MYC-driven tumors (Grp3-MB) still suffer significant morbidity and mortality. There is an urgent need to explore multimodal therapeutic regimens which are effective and safe for children. Large-scale studies have revealed abnormal cancer epigenomes caused by mutations and structural alterations of chromatin modifiers, aberrant DNA methylation, and histone modification signatures. Therefore, targeting epigenetic modifiers for cancer treatment has gained increasing interest, and inhibitors for various epigenetic modulators have been intensively studied in clinical trials. Here, we report a cross-entity, epigenetic drug screen to "],"journal":["Journal for immunotherapy of cancer"],"pubmed_title":["Tacedinaline (CI-994), a class I HDAC inhibitor, targets intrinsic tumor growth and leptomeningeal dissemination in MYC-driven medulloblastoma while making them susceptible to anti-CD47-induced macrophage phagocytosis via NF-kB-TGM2 driven tumor inflammation."],"pmcid":["PMC9843227"],"funding_grant_id":["N/A","P30-CA046934","110663","V2021-013","S10 OD027023","25B0712","612617","01ZX1401B","P30 CA014236","111537","70112951","2380102","P30 CA046934","P-91650709","S10 OD023485","16-184-56","03VP0731"],"pubmed_authors":["Qin N","Maue M","Hansen FK","Picard D","Cole A","Pauck D","Bartl J","Remke M","Langini M","Borkhardt A","Blumel L","Witt O","Beez T","Kahlert U","Theruvath J","Ahmadov U","Venkatraman S","Stefanski A","Mitra S","Bigner DD","Fischer U","Reifenberger G","Leprivier G","Cheshier SH","Kurz T","Milde T","Erdreich-Epstein A","Marquardt V","Graef CM","Wolfl M","Hauer J","Knobbe-Thomsen CB","Keir ST","Vibhakar R","Felsberg J","Cruz-Cruz J","Stuhler K","Meyer FD"],"additional_accession":[]},"is_claimable":false,"name":"Tacedinaline (CI-994), a class I HDAC inhibitor, targets intrinsic tumor growth and leptomeningeal dissemination in MYC-driven medulloblastoma while making them susceptible to anti-CD47-induced macrophage phagocytosis via NF-kB-TGM2 driven tumor inflammation.","description":"<h4>Background</h4>While major advances have been made in improving the quality of life and survival of children with most forms of medulloblastoma (MB), those with MYC-driven tumors (Grp3-MB) still suffer significant morbidity and mortality. There is an urgent need to explore multimodal therapeutic regimens which are effective and safe for children. Large-scale studies have revealed abnormal cancer epigenomes caused by mutations and structural alterations of chromatin modifiers, aberrant DNA methylation, and histone modification signatures. Therefore, targeting epigenetic modifiers for cancer treatment has gained increasing interest, and inhibitors for various epigenetic modulators have been intensively studied in clinical trials. Here, we report a cross-entity, epigenetic drug screen to ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2026-06-13T06:20:16.346Z","creation":"2024-11-15T20:05:11.916Z"},"accession":"S-EPMC9843227","cross_references":{"pubmed":["36639156"],"doi":["10.1136/jitc-2022-005871"]}}