{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Theruvath J"],"funding":["Children with Cancer UK","NCI NIH HHS","NINDS NIH HHS","The Brain Tumour Charity"],"pagination":["712-719"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7992505"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(5)"],"pubmed_abstract":["Atypical teratoid/rhabdoid tumors (ATRTs) typically arise in the central nervous system (CNS) of children under 3 years of age. Despite intensive multimodal therapy (surgery, chemotherapy and, if age permits, radiotherapy), median survival is 17 months<sup>1,2</sup>. We show that ATRTs robustly express B7-H3/CD276 that does not result from the inactivating mutations in SMARCB1 (refs. <sup>3,4</sup>), which drive oncogenesis in ATRT, but requires residual SWItch/Sucrose Non-Fermentable (SWI/SNF) activity mediated by BRG1/SMARCA4. Consistent with the embryonic origin of ATRT<sup>5,6</sup>, B7-H3 is highly expressed on the prenatal, but not postnatal, brain. B7-H3.BB.z-chimeric antigen receptor (CAR) T cells administered intracerebroventricularly or intratumorally mediate potent antitumor eff"],"journal":["Nature medicine"],"pubmed_title":["Locoregionally administered B7-H3-targeted CAR T cells for treatment of atypical teratoid/rhabdoid tumors."],"pmcid":["PMC7992505"],"funding_grant_id":["P30 CA124435","12-134","R25 NS065741","16/193"],"pubmed_authors":["Mount CW","Kool M","Finetti MA","Labanieh L","Bourdeaut F","Dhingra S","Pfister S","Johann PD","Williamson D","Theruvath J","Zaidi S","Mackall CL","Sorensen PH","Xu P","Yecies DW","Delaidelli A","Majzner RG","Cheshier S","Graef CM","Puget S","Sotillo E","Heitzeneder S","Leruste A","Mitra SS","Hasselblatt M","Mueller S","Fruhwald MC","Monje M","Surdez D","Delattre O"],"additional_accession":[]},"is_claimable":false,"name":"Locoregionally administered B7-H3-targeted CAR T cells for treatment of atypical teratoid/rhabdoid tumors.","description":"Atypical teratoid/rhabdoid tumors (ATRTs) typically arise in the central nervous system (CNS) of children under 3 years of age. Despite intensive multimodal therapy (surgery, chemotherapy and, if age permits, radiotherapy), median survival is 17 months<sup>1,2</sup>. We show that ATRTs robustly express B7-H3/CD276 that does not result from the inactivating mutations in SMARCB1 (refs. <sup>3,4</sup>), which drive oncogenesis in ATRT, but requires residual SWItch/Sucrose Non-Fermentable (SWI/SNF) activity mediated by BRG1/SMARCA4. Consistent with the embryonic origin of ATRT<sup>5,6</sup>, B7-H3 is highly expressed on the prenatal, but not postnatal, brain. B7-H3.BB.z-chimeric antigen receptor (CAR) T cells administered intracerebroventricularly or intratumorally mediate potent antitumor eff","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2026-05-02T11:27:07.85Z","creation":"2025-04-05T17:16:28.16Z"},"accession":"S-EPMC7992505","cross_references":{"pubmed":["32341579"],"doi":["10.1038/s41591-020-0821-8"]}}