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- W4313366264 abstract "Abstract Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second leading cause of cancer related death in the U.S. by 2030. Being completely refractory to checkpoint therapies, management of PDAC remains an unmet clinical need. Intriguingly, the human protein atlas (THPA) shows elevated mRNA expression of vasoactive intestinal peptide (VIP), a neurotransmitter in exocrine pancreatic cancers. Interestingly, VIP also has immunosuppressive properties leading to decreased T cell proliferation and enhanced expansion of myeloid derived suppressor cells (MDSCs) and regulatory T cells (Tregs). Thus, we are investigating the role of VIP in PDAC progression and the effect of inhibiting VIP signaling for improved responsiveness to immunotherapy. We found that consistent with THPA, cell culture supernatants collected from murine PDAC cell lines had significantly higher levels of VIP as compared to melanoma and breast cancer cells. Similarly, elevated levels of VIP were observed in mice bearing PDAC tumors, and in plasma from human PDAC patients, when compared to naïve mice and healthy volunteer samples, respectively. Treatment of immune competent mice bearing PDAC tumors (MT5 or KPC cell lines) with the combination of a VIP antagonist (VIPhyb) and anti-PD1, produced complete and durable regression of tumors in 20% of the mice and an overall delayed tumor progression in both tumor models. Upon analysis of the tumor tissues sections via immunohistochemistry, significant infiltration of CD8+ T cells was observed in mice treated with the combination of VIPhyb and anti-PD1. Further experiments are underway to understand the mechanism of action of VIP antagonist and to devise methods to improve its efficacy in-vivo." @default.
- W4313366264 created "2023-01-06" @default.
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- W4313366264 date "2019-05-01" @default.
- W4313366264 modified "2023-09-26" @default.
- W4313366264 title "Vasoactive intestinal peptide signaling – a novel immune checkpoint in pancreatic ductal adenocarcinoma" @default.
- W4313366264 doi "https://doi.org/10.4049/jimmunol.202.supp.70.8" @default.
- W4313366264 hasPublicationYear "2019" @default.
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