{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Stromnes IM"],"funding":["AACR","American Cancer Society","NIAID NIH HHS","Pancreatic Cancer Action Network","National Cancer Institute","NCI NIH HHS","Giles W. and Elise G. Mead Foundation","Cancer Center"],"pagination":["977-989"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6548612"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(6)"],"pubmed_abstract":["Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy resistant to therapies, including immune-checkpoint blockade. We investigated two distinct strategies to modulate tumor-associated macrophages (TAM) to enhance cellular therapy targeting mesothelin in an autochthonous PDA mouse model. Administration of an antibody to colony-stimulating factor (anti-Csf1R) depleted Ly6C<sup>low</sup> protumorigenic TAMs and significantly enhanced endogenous T-cell intratumoral accumulation. Despite increasing the number of endogenous T cells at the tumor site, as previously reported, TAM depletion had only minimal impact on intratumoral accumulation and persistence of T cells engineered to express a murine mesothelin-specific T-cell receptor (TCR). TAM depletion interfered with the antitumor acti"],"journal":["Cancer immunology research"],"pubmed_title":["Differential Effects of Depleting versus Programming Tumor-Associated Macrophages on Engineered T Cells in Pancreatic Ductal Adenocarcinoma."],"pmcid":["PMC6548612"],"funding_grant_id":["P30 CA015704","CA018029","R01 CA161112","124166-IRG-58-001-55-IRG65","CA033084","P30CA015704","CA161112","T35 AI118620","P01 CA018029","R37 CA033084","17-20-25-STRO","16-65-GREE","R01 CA033084"],"pubmed_authors":["Raynor JF","Greenberg PD","Spartz EJ","Pierce RH","Hingorani SR","Burrack AL","Hulbert A","Brockenbrough JS","Stromnes IM","Black C","Bonson P"],"additional_accession":[]},"is_claimable":false,"name":"Differential Effects of Depleting versus Programming Tumor-Associated Macrophages on Engineered T Cells in Pancreatic Ductal Adenocarcinoma.","description":"Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy resistant to therapies, including immune-checkpoint blockade. We investigated two distinct strategies to modulate tumor-associated macrophages (TAM) to enhance cellular therapy targeting mesothelin in an autochthonous PDA mouse model. Administration of an antibody to colony-stimulating factor (anti-Csf1R) depleted Ly6C<sup>low</sup> protumorigenic TAMs and significantly enhanced endogenous T-cell intratumoral accumulation. Despite increasing the number of endogenous T cells at the tumor site, as previously reported, TAM depletion had only minimal impact on intratumoral accumulation and persistence of T cells engineered to express a murine mesothelin-specific T-cell receptor (TCR). TAM depletion interfered with the antitumor acti","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-04-04T07:58:04.043Z","creation":"2020-06-04T07:06:57Z"},"accession":"S-EPMC6548612","cross_references":{"pubmed":["31028033"],"doi":["10.1158/2326-6066.cir-18-0448","10.1158/2326-6066.CIR-18-0448"]}}