{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Watanabe J"],"funding":["Pediatric Cancer Research Foundation","Rally Foundation","Matthew Larson Foundation for Pediatric Brain Tumors","Cure Starts Now Foundation","NCI NIH HHS","NINDS NIH HHS","National Institutes of Health","Japan Society for the Promotion of Science"],"pagination":["e174794"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11213469"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(13)"],"pubmed_abstract":["Diffuse midline glioma (DMG) H3K27-altered is one of the most malignant childhood cancers. Radiation therapy remains the only effective treatment yet provides a 5-year survival rate of only 1%. Several clinical trials have attempted to enhance radiation antitumor activity using radiosensitizing agents, although none have been successful. Given this, there is a critical need for identifying effective therapeutics to enhance radiation sensitivity for the treatment of DMG. Using high-throughput radiosensitivity screening, we identified bromo- and extraterminal domain (BET) protein inhibitors as potent radiosensitizers in DMG cells. Genetic and pharmacologic inhibition of BET bromodomain activity reduced DMG cell proliferation and enhanced radiation-induced DNA damage by inhibiting DNA repair "],"journal":["The Journal of clinical investigation"],"pubmed_title":["BET bromodomain inhibition potentiates radiosensitivity in models of H3K27-altered diffuse midline glioma."],"pmcid":["PMC11213469"],"funding_grant_id":["P50 CA221747","N/A","22IC36","R01 NS126513","R01CA197313","5P50CA221747","R01NS126513","R01 CA277605","R01 CA258636","R01CA258636","R01 CA197313","R01 CA204297","R01 NS093079","863193","R01 NS132344","R01NS132344"],"pubmed_authors":["Gadd S","Clutter MR","Natsumeda M","Sasaki T","Uchida E","Abe K","Kaur S","Ishi Y","Watanabe J","Zhang Z","Becher OJ","Gullette MJ","Takata N","Mo Y","Hashizume R"],"additional_accession":[]},"is_claimable":false,"name":"BET bromodomain inhibition potentiates radiosensitivity in models of H3K27-altered diffuse midline glioma.","description":"Diffuse midline glioma (DMG) H3K27-altered is one of the most malignant childhood cancers. Radiation therapy remains the only effective treatment yet provides a 5-year survival rate of only 1%. Several clinical trials have attempted to enhance radiation antitumor activity using radiosensitizing agents, although none have been successful. Given this, there is a critical need for identifying effective therapeutics to enhance radiation sensitivity for the treatment of DMG. Using high-throughput radiosensitivity screening, we identified bromo- and extraterminal domain (BET) protein inhibitors as potent radiosensitizers in DMG cells. Genetic and pharmacologic inhibition of BET bromodomain activity reduced DMG cell proliferation and enhanced radiation-induced DNA damage by inhibiting DNA repair ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-07-15T12:00:49.401Z","creation":"2026-07-04T03:12:02.63Z"},"accession":"S-EPMC11213469","cross_references":{"pubmed":["38771655"],"doi":["10.1172/JCI174794"]}}