{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Satta A"],"funding":["AIRC 5 × 1000","AIRC"],"pagination":["1084-1097"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6204841"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(7)"],"pubmed_abstract":["Recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or TRAIL-receptor agonistic monoclonal antibodies promote apoptosis in most cancer cells, and the differential expression of TRAIL-R2 between tumor and normal tissues allows its exploitation as a tumor-associated antigen. The use of these antibodies as anticancer agents has been extensively studied, but the results of clinical trials were disappointing. The observed lack of anticancer activity could be attributed to intrinsic or acquired resistance of tumor cells to this type of treatment. A possible strategy to circumvent drug resistance would be to strike tumor cells with a second modality based on a different mechanism of action. We therefore set out to generate and optimize a bispecific antibody targeting"],"journal":["mAbs"],"pubmed_title":["Design, selection and optimization of an anti-TRAIL-R2/anti-CD3 bispecific antibody able to educate T cells to recognize and destroy cancer cells."],"pmcid":["PMC6204841"],"funding_grant_id":["MCO9998"],"pubmed_authors":["Satta A","Desideri A","Anichini A","Di Nicola M","Kontermann RE","Frigerio B","Figini M","Gianni AM","Mezzanzanica D","Caroli F","Iacovelli F","Canevari S"],"additional_accession":[]},"is_claimable":false,"name":"Design, selection and optimization of an anti-TRAIL-R2/anti-CD3 bispecific antibody able to educate T cells to recognize and destroy cancer cells.","description":"Recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or TRAIL-receptor agonistic monoclonal antibodies promote apoptosis in most cancer cells, and the differential expression of TRAIL-R2 between tumor and normal tissues allows its exploitation as a tumor-associated antigen. The use of these antibodies as anticancer agents has been extensively studied, but the results of clinical trials were disappointing. The observed lack of anticancer activity could be attributed to intrinsic or acquired resistance of tumor cells to this type of treatment. A possible strategy to circumvent drug resistance would be to strike tumor cells with a second modality based on a different mechanism of action. We therefore set out to generate and optimize a bispecific antibody targeting","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2025-04-26T23:01:08.385Z","creation":"2019-08-09T07:02:29Z"},"accession":"S-EPMC6204841","cross_references":{"pubmed":["29993310"],"doi":["10.1080/19420862.2018.1494105"]}}