Blockade of fibroblast activation protein in combination with radiation treatment in murine models of pancreatic adenocarcinoma
Andrew J. Gunderson; Tomoko Yamazaki; Kayla McCarty; Michaela Phillips; Alejandro Alice; Shelly Bambina; Lauren Zebertavage; David J. Friedman · 2019 · PLoS ONE
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a fibrotic stroma with a poor lymphocyte infiltrate, in part driven by cancer-associated fibroblasts (CAFs). CAFs, which express fibroblast activation protein (FAP), contribute to immune escape via exclusion of anti-tumor CD8+ T cells from cancer cells, upregulation of immune checkpoint ligand expression, immunosuppressive cytokine production, and polarization of tumor infiltrating inflammatory cells. FAP is a post-proline peptidase selectively expressed during tissue remodeling and repair, such as with wound healing, and in the tumor
Abstract by Andrew J. Gunderson; Tomoko Yamazaki; Kayla McCarty; Michaela Phillips; Alejandro Alice; Shelly Bambina; Lauren Zebertavage; David J. Friedman, PLoS ONE (2019) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1371/journal.pone.0211117