RNAi-Mediated PD-L1 Inhibition for Pancreatic Cancer Immunotherapy View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Byunghee Yoo, Veronica Clavijo Jordan, Patrick Sheedy, Ann-Marie Billig, Alana Ross, Pamela Pantazopoulos, Zdravka Medarova

ABSTRACT

The recent past has seen impressive progress in the treatment of various malignancies using immunotherapy. One of the most promising approaches involves immune checkpoint inhibitors. However, the clinical results with these agents have demonstrated variability in the response. Pancreatic cancer, in particular, has proven resistant to initial immunotherapy approaches. Here, we describe an alternative strategy that relies on combining gemcitabine and a novel programmed death-ligand 1 (PD-L1) inhibitor, termed MN-siPDL1. MN-siPDL1 incorporates small interfering RNA against PD-L1 (siPDL1) conjugated to a magnetic nanocarrier (MN). We show that noninvasive magnetic resonance imaging (MRI) could be used to monitor therapeutic response. Combination therapy consisting of gemcitabine and MN-siPDL1 in a syngeneic murine pancreatic cancer model resulted in a significant reduction in tumor growth and an increase in survival. Following optimization, a 90% reduction in tumor volume was achieved 2 weeks after the beginning of treatment. Whereas 100% of the control animals had succumbed to their tumors by week 6 after the beginning of treatment, there was no mortality in the experimental group by week 5, and 67% of the experimental animals survived for 12 weeks. This method could provide therapeutic benefit against an intractable disease for which there are no effective treatments and which is characterized by a mere 1% 5-year survival. More... »

PAGES

4712

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-019-41251-9

DOI

http://dx.doi.org/10.1038/s41598-019-41251-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112849854

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30886310


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