{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Maso L"],"funding":["HHS | NIH | National Cancer Institute","NCI NIH HHS","HHS | NIH | National Cancer Institute (NCI)"],"pagination":["e2509012122"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12337345"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122(31)"],"pubmed_abstract":["Effective immune therapy against cancer ideally should target a cancer-specific antigen, an antigen that is present exclusively in cancer cells. However, there is a paucity of cancer-specific antigens that are endogenously produced. HapImmune™ technology utilizes covalent inhibitors directed to an intracellular cancer driver to create cancer-specific neoantigens in the form of drug-peptide conjugates presented by class I MHC molecules. Our previous study with sotorasib, an FDA-approved covalent inhibitor of KRAS(G12C), demonstrated that drug-treated cells produce such neoantigens and can be killed by T cell engagers directed against the drug-peptide/MHC complex. Thus, this technology can unite targeted and immune therapies. In the present study, we examined whether this approach could gene"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Generation of actionable, cancer-specific neoantigens from KRAS(G12C) with adagrasib."],"pmcid":["PMC12337345"],"funding_grant_id":["R21CA267362","P30CA016087","P30 CA016087","R01 CA248896","R01CA248896","R21 CA267362"],"pubmed_authors":["Rajak E","Koide A","Hu Z","Hattori T","Neel BG","Koide S","Maso L"],"additional_accession":[]},"is_claimable":false,"name":"Generation of actionable, cancer-specific neoantigens from KRAS(G12C) with adagrasib.","description":"Effective immune therapy against cancer ideally should target a cancer-specific antigen, an antigen that is present exclusively in cancer cells. However, there is a paucity of cancer-specific antigens that are endogenously produced. HapImmune™ technology utilizes covalent inhibitors directed to an intracellular cancer driver to create cancer-specific neoantigens in the form of drug-peptide conjugates presented by class I MHC molecules. Our previous study with sotorasib, an FDA-approved covalent inhibitor of KRAS(G12C), demonstrated that drug-treated cells produce such neoantigens and can be killed by T cell engagers directed against the drug-peptide/MHC complex. Thus, this technology can unite targeted and immune therapies. In the present study, we examined whether this approach could gene","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-06-16T07:08:51.893Z","creation":"2026-06-16T03:09:41.93Z"},"accession":"S-EPMC12337345","cross_references":{"pubmed":["40737322"],"doi":["10.1073/pnas.2509012122"]}}