{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(4)"],"submitter":["Rozenbaum M"],"funding":["Varda and Boaz Dotan Research Center for Hemato-Oncology Research, Tel Aviv University (Dotan Research Center in Hemato-Oncology, Tel Aviv University)","Varda and Boaz Dotan Research Center for Hemato-Oncology Research, Tel Aviv University","Action for A-T (Action for AT)","Action for A-T"],"pubmed_abstract":["Somatic variants in DNA damage response genes such as ATM are widespread in hematologic malignancies. ATM protein is essential for double-strand DNA break repair. Germline ATM deficiencies underlie ataxia-telangiectasia (A-T), a disease manifested by radiosensitivity, immunodeficiency, and predisposition to lymphoid malignancies. Patients with A-T diagnosed with malignancies have poor tolerance to chemotherapy or radiation. In this study, we investigated chimeric antigen receptor (CAR) T cells using primary T cells from patients with A-T (ATM-/-), heterozygote donors (ATM+/-), and healthy donors. ATM-/- T cells proliferate and can be successfully transduced with CARs, though functional impairment of ATM-/- CAR T-cells was observed. Retroviral transduction of the CAR in ATM-/- T cells resul"],"journal":["Blood cancer discovery"],"pagination":["267-275"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11215369"],"repository":["biostudies-literature"],"pubmed_title":["Genotoxicity Associated with Retroviral CAR Transduction of ATM-Deficient T Cells."],"pmcid":["PMC11215369"],"pubmed_authors":["Zinger T","Rechavi G","Jacoby E","Sarouk I","Saar EG","Fluss R","Meir A","Elitzur S","Rozenbaum M","Marcu-Malina V","Jacob-Hirsch J"],"additional_accession":[]},"is_claimable":false,"name":"Genotoxicity Associated with Retroviral CAR Transduction of ATM-Deficient T Cells.","description":"Somatic variants in DNA damage response genes such as ATM are widespread in hematologic malignancies. ATM protein is essential for double-strand DNA break repair. Germline ATM deficiencies underlie ataxia-telangiectasia (A-T), a disease manifested by radiosensitivity, immunodeficiency, and predisposition to lymphoid malignancies. Patients with A-T diagnosed with malignancies have poor tolerance to chemotherapy or radiation. In this study, we investigated chimeric antigen receptor (CAR) T cells using primary T cells from patients with A-T (ATM-/-), heterozygote donors (ATM+/-), and healthy donors. ATM-/- T cells proliferate and can be successfully transduced with CARs, though functional impairment of ATM-/- CAR T-cells was observed. Retroviral transduction of the CAR in ATM-/- T cells resul","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-02T12:08:16.514Z","creation":"2026-04-18T03:10:59.364Z"},"accession":"S-EPMC11215369","cross_references":{"pubmed":["38747501"],"doi":["10.1158/2643-3230.bcd-23-0268","10.1158/2643-3230.BCD-23-0268"]}}