{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Supper VM"],"funding":["National Cancer Institute (NCI)","American Cancer Society","National Cancer Institute","NCI NIH HHS","American Cancer Society (ACS)"],"pagination":["1132-1144"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12777652"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(8)"],"pubmed_abstract":["Chimeric antigen receptor (CAR) T-cell therapy is an effective treatment strategy for B-cell malignancies; however, its efficacy in solid tumors remains limited. VEGF-targeted drugs are used as antitumor agents to target abnormal tumor vasculature; however, toxicities associated with systemic VEGF blockade limit their maximal therapeutic benefit. Increasing evidence suggests a role for VEGF in the immunosuppressive tumor microenvironment, including through direct induction of T cell-effector dysfunction. In this study, we show that CAR T cells from patients treated with FDA-approved CAR T-cell products express members of the VEGF signaling pathway, and this expression is correlated with patient nonresponse. To overcome putative VEGF-induced CAR T-cell dysfunction and deliver local VEGF blo"],"journal":["Cancer immunology research"],"pubmed_title":["Secretion of a VEGF-Blocking scFv Enhances CAR T-cell Potency."],"pmcid":["PMC12777652"],"funding_grant_id":["K08 CA289948-02","K08 CA289948","R01 CA238268","YACS-24-1334735-01-YACS"],"pubmed_authors":["Leick MB","Bratt A","Birocchi F","Choi BD","Korell F","Philips M","Park S","Takei H","Parker A","Armstrong A","Martin G","Kienka T","Donner H","Bouffard A","Salas-Benito D","Goncalves S","Kann MC","Maus MV","Supper VM","Escobar G","Bailey SR","Haradhvala NJ","Darnell EP"],"additional_accession":[]},"is_claimable":false,"name":"Secretion of a VEGF-Blocking scFv Enhances CAR T-cell Potency.","description":"Chimeric antigen receptor (CAR) T-cell therapy is an effective treatment strategy for B-cell malignancies; however, its efficacy in solid tumors remains limited. VEGF-targeted drugs are used as antitumor agents to target abnormal tumor vasculature; however, toxicities associated with systemic VEGF blockade limit their maximal therapeutic benefit. Increasing evidence suggests a role for VEGF in the immunosuppressive tumor microenvironment, including through direct induction of T cell-effector dysfunction. In this study, we show that CAR T cells from patients treated with FDA-approved CAR T-cell products express members of the VEGF signaling pathway, and this expression is correlated with patient nonresponse. To overcome putative VEGF-induced CAR T-cell dysfunction and deliver local VEGF blo","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-06-06T12:37:33.802Z","creation":"2026-05-30T03:11:26.627Z"},"accession":"S-EPMC12777652","cross_references":{"pubmed":["40455064"],"doi":["10.1158/2326-6066.cir-24-0876","10.1158/2326-6066.CIR-24-0876"]}}