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• W2897465705 startingPage "348" @default.
• W2897465705 abstract "Abstract Resistance to standard therapy remains a major challenge in the treatment of pancreatic ductal adenocarcinoma (PDA). Although anti-VEGF therapy delays PDA progression, therapy-induced hypoxia results in a less differentiated mesenchymal-like tumor cell phenotype, which reinforces the need for effective companion therapies. COX-2 inhibition has been shown to promote tumor cell differentiation and improve standard therapy response in PDA. Here, we evaluate the efficacy of COX-2 inhibition and VEGF blockade in preclinical models of PDA. In vivo, the combination therapy was more effective in limiting tumor growth and metastasis than single-agent therapy. Combination therapy also reversed anti-VEGF–induced epithelial–mesenchymal transition and collagen deposition and altered the immune landscape by increasing tumor-associated CD8+ T cells while reducing FoxP3+ T cells and FasL expression on the tumor endothelium. Implications: Together, these findings demonstrate that COX-2 inhibition enhances the efficacy of anti-VEGF therapy by reducing hypoxia-induced epithelial plasticity and promoting an immune landscape that might facilitate immune activation. Visual Overview: http://mcr.aacrjournals.org/content/molcanres/17/2/348/F1.large.jpg." @default.
• W2897465705 created "2018-10-26" @default.
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• W2897465705 date "2019-02-01" @default.
• W2897465705 modified "2023-10-17" @default.
• W2897465705 title "Cyclooxygenase-2 Inhibition Potentiates the Efficacy of Vascular Endothelial Growth Factor Blockade and Promotes an Immune Stimulatory Microenvironment in Preclinical Models of Pancreatic Cancer" @default.
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• W2897465705 doi "https://doi.org/10.1158/1541-7786.mcr-18-0427" @default.
• W2897465705 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6359969" @default.
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• W2897465705 hasPublicationYear "2019" @default.
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