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- W2945115405 abstract "The presence of tumor-infiltrating T cells is associated with favorable patient outcomes, yet most pancreatic cancers are immunologically silent and resistant to currently available immunotherapies. Here we show using a syngeneic orthotopic implantation model of pancreatic cancer that Pik3ca regulates tumor immunogenicity. Genetic silencing of Pik3ca in KrasG12D/Trp53R172H-driven pancreatic tumors resulted in infiltration of T cells, complete tumor regression, and 100% survival of immunocompetent host mice. By contrast, Pik3ca-null tumors implanted in T cell-deficient mice progressed and killed all of the animals. Adoptive transfer of tumor antigen-experienced T cells eliminated Pik3ca-null tumors in immunodeficient mice. Loss of PIK3CA or inhibition of its effector, AKT, increased the expression of MHC Class I and CD80 on tumor cells. These changes contributed to the increased susceptibility of Pik3ca-null tumors to T cell surveillance. Our results indicate that tumor cell PIK3CA-AKT signaling limits T cell recognition and clearance of pancreatic cancer cells. Strategies that target this pathway may yield an effective immunotherapy for this cancer." @default.
- W2945115405 created "2019-05-29" @default.
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- W2945115405 date "2019-07-15" @default.
- W2945115405 modified "2023-10-03" @default.
- W2945115405 title "Tumor-intrinsic PIK3CA represses tumor immunogenicity in a model of pancreatic cancer" @default.
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- W2945115405 doi "https://doi.org/10.1172/jci123540" @default.
- W2945115405 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6668699" @default.
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- W2945115405 hasPublicationYear "2019" @default.
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