Prostaglandin E2 promotes tumor progression by inducing myeloid-derived suppressor cells.
By P. Sinha, V. Clements, A. Fulton, S. Ostrand-Rosenberg. Cancer Research, 2007
754 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/541c5d3599795b8ea0cb109e34f25a25d3f851ac
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Citations in the corpus
- Proinflammatory S100 Proteins Regulate the Accumulation of Myeloid-Derived Suppressor Cells (2008, background): “Inflammation is an inducer of MDSC (8, 10, 11).”
- Eicosanoids and cancer (2010, background): “Furthermore, PGE 2 promoted mammary tumour progression through the induction of MDSCs in vivo”
- Molecular mechanisms regulating myeloid-derived suppressor cell differentiation and function (2010, background): “EP receptor agonists, including PGE2, induced the generation of MDSC from bone marrow stem cells; whereas, receptor antagonists blocked differentiation[64].”
- Myeloid derived suppressor cells (2013, background): “43 In a positive feedback cycle, these skewed macrophages can then induce further IL-10 production by MDSCs. MDSC-directed immunosuppression often extends to other cells as well.”
- Coordinated regulation of myeloid cells by tumours (2012, positive): “Tumour-derived TGFβ also regulates MDSC accumulatio”
- Myeloid-derived-suppressor cells as regulators of the immune system (2009, positive): “Factors that induce MDSC expansion can include cyclooxygenase 2 (also known as PTGS2), prostaglandin”
- Induction of myeloid-derived suppressor cells by tumor exosomes (2009, background): “These proteins could also play a role in exosome-mediated induction of MDSCs.”
- Reduced inflammation in the tumor microenvironment delays the accumulation of myeloid-derived suppressor cells and limits tumor progression. (2007, methodology): “We have recently proposed that immune suppression may be one of these mechanisms, and have hypothesized that chronic inflammation causes immune suppression, which inhibits immune surveillance and/or tumor immunity thereby enhancing the proliferation of malignant cells (3, 4).”
- Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, background): “Furthermore, IL-1β upregulated COX-2, which encodes prostaglandins that are responsible for MDSCs expansion.(309) Tissue-resident endothelial cells are activated by MDSCs to produce VEGF and other angiogenic factors with the stimulation of IL-1β and other pro-inflammatory agents.”
- Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer (2009, background): “Therefore, similarly as IL-1 , IL-6, and PGE2, S100A8/A9 proteins facilitate the accumulation of MDSC.”