DMXAA Causes Tumor Site-Specific Vascular Disruption in Murine Non-Small Cell Lung Cancer, and like the Endogenous Non-Canonical Cyclic Dinucleotide STING Agonist, 2′3′-cGAMP, Induces M2 Macrophage Repolarization

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M. Downey, Charlene; Aghaei, Mehrnoosh; A. Schwendener, Reto; Jirik, Frank R.;
  • Publisher: Figshare
  • Related identifiers: doi: 10.1371/journal.pone.0099988
  • Subject: Biological Sciences | immunology | Clinical immunology | immunotherapy | oncology | Basic cancer research | metastasis | Cancers and neoplasms | carcinomas | adenocarcinomas | Adenocarcinoma of the lung | Lung and intrathoracic tumors | Non-small cell lung cancer | Cancer treatment | Antiangiogenesis therapy | Animal studies | Animal models of disease | Model organisms | Animal models | Mouse models | research design | Clinical research design | causes | site-specific | vascular | disruption | murine | non-small | endogenous | non-canonical | cyclic | dinucleotide | sting | m2 | macrophage

<div><p>The vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA), a murine agonist of the stimulator of interferon genes (STING), appears to target the tumor vasculature primarily as a result of stimulating pro-inflammatory cytokine production from tum... View more
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