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- W2969704706 abstract "<h2>Summary</h2> Pancreatic ductal adenocarcinoma (PDA) is a lethal cancer resistant to immunotherapy. We create a PDA mouse model and show that neoantigen expression is required for intratumoral T cell accumulation and response to immune checkpoint blockade. By generating a peptide:MHC tetramer, we identify that PDA induces rapid intratumoral, and progressive systemic, tumor-specific T cell exhaustion. Monotherapy PD-1 or PD-L1 blockade enhances systemic T cell expansion and induces objective responses that require systemic T cells. However, tumor escape variants defective in IFNγ-inducible <i>Tap1</i> and MHC class I cell surface expression ultimately emerge. Combination PD-1 + PD-L1 blockade synergizes therapeutically by increasing intratumoral KLRG1+Lag3−TNFα+ tumor-specific T cells and generating memory T cells capable of expanding to spontaneous tumor recurrence, thereby prolonging animal survival. Our studies support that PD-1 and PD-L1 are relevant immune checkpoints in PDA and identify a combination for clinical testing in those patients with neoantigen-specific T cells." @default.
- W2969704706 created "2019-08-29" @default.
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- W2969704706 creator A5069622917 @default.
- W2969704706 date "2019-08-01" @default.
- W2969704706 modified "2023-10-16" @default.
- W2969704706 title "Combination PD-1 and PD-L1 Blockade Promotes Durable Neoantigen-Specific T Cell-Mediated Immunity in Pancreatic Ductal Adenocarcinoma" @default.
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- W2969704706 doi "https://doi.org/10.1016/j.celrep.2019.07.059" @default.
- W2969704706 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7975822" @default.
- W2969704706 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31433988" @default.
- W2969704706 hasPublicationYear "2019" @default.
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