{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shafer P"],"funding":["NHLBI NIH HHS","NCI NIH HHS","NIGMS NIH HHS","NIH HHS"],"pagination":["266-275"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10922969"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(3)"],"pubmed_abstract":["T cell receptor engineered T cell (TCR T) therapies have shown recent efficacy against certain types of solid metastatic cancers. However, to extend TCR T therapies to treat more patients across additional cancer types, new TCRs recognizing cancer-specific antigen targets are needed. Driver mutations in AKT1, ESR1, PIK3CA, and TP53 are common in patients with metastatic breast cancer (MBC) and if immunogenic could serve as ideal tumor-specific targets for TCR T therapy to treat this disease. Through IFN-γ ELISpot screening of in vitro expanded neopeptide-stimulated T cell lines from healthy donors and MBC patients, we identified reactivity towards 11 of 13 of the mutations. To identify neopeptide-specific TCRs, we then performed single-cell RNA sequencing of one of the T cell lines followi"],"journal":["Cytotherapy"],"pubmed_title":["Incongruity between T cell receptor recognition of breast cancer hotspot mutations ESR1 Y537S and D538G following exogenous peptide loading versus endogenous antigen processing."],"pmcid":["PMC10922969"],"funding_grant_id":["S10 OD025240","R01 CA072038","T32 GM136554","T32 HL092332","P50 CA058183","S10 OD023469","R37 CA248478"],"pubmed_authors":["Woods M","Choi JM","Rodriguez-Plata CM","Rooney C","Maknojia A","Shafer P","Fuqua S","Hoyos V","Leung WK","Manliguez A","Burt B","Lee HS","Mosquera A","Somes LK","Joubert J","Zhang B","Leen AM","Ranjan R"],"additional_accession":[]},"is_claimable":false,"name":"Incongruity between T cell receptor recognition of breast cancer hotspot mutations ESR1 Y537S and D538G following exogenous peptide loading versus endogenous antigen processing.","description":"T cell receptor engineered T cell (TCR T) therapies have shown recent efficacy against certain types of solid metastatic cancers. However, to extend TCR T therapies to treat more patients across additional cancer types, new TCRs recognizing cancer-specific antigen targets are needed. Driver mutations in AKT1, ESR1, PIK3CA, and TP53 are common in patients with metastatic breast cancer (MBC) and if immunogenic could serve as ideal tumor-specific targets for TCR T therapy to treat this disease. Through IFN-γ ELISpot screening of in vitro expanded neopeptide-stimulated T cell lines from healthy donors and MBC patients, we identified reactivity towards 11 of 13 of the mutations. To identify neopeptide-specific TCRs, we then performed single-cell RNA sequencing of one of the T cell lines followi","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-04T00:48:07.914Z","creation":"2025-04-04T00:48:07.914Z"},"accession":"S-EPMC10922969","cross_references":{"pubmed":["38231165"],"doi":["10.1016/j.jcyt.2023.12.002"]}}