Abstract
We found a shared immunosuppressive microenvironment between foetal liver and hepatocellular carcinoma (HCC) which includes the re-emergence of foetal-associated endothelial cells (PLVAP/VEGFR2) and foetal-like (FOLR2) tumour-associated macrophages in HCC, mediated via VEGF-NOTCH signalling. The discoveries suggest possible novel targets for therapeutic interventions in HCC.
MeSH terms
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Animals
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / immunology
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Carcinoma, Hepatocellular / pathology*
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / immunology
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Cellular Reprogramming / genetics
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Cellular Reprogramming / immunology
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Fetal Development / genetics
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Fetal Development / immunology
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Folate Receptor 2 / physiology
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Humans
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Liver Neoplasms / genetics
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Liver Neoplasms / immunology
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Liver Neoplasms / pathology*
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Macrophages / pathology
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Macrophages / physiology
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Membrane Proteins / genetics
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Membrane Proteins / physiology
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Mice
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Signal Transduction / genetics
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Signal Transduction / immunology
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Tumor Escape* / genetics
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Tumor Escape* / immunology
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Tumor Microenvironment / genetics
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Tumor Microenvironment / immunology
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Vascular Endothelial Growth Factor Receptor-2 / genetics
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Vascular Endothelial Growth Factor Receptor-2 / physiology
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alpha-Fetoproteins / genetics
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alpha-Fetoproteins / physiology
Substances
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FOLR2 protein, human
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Folate Receptor 2
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Membrane Proteins
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PLVAP protein, human
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alpha-Fetoproteins
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KDR protein, human
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Vascular Endothelial Growth Factor Receptor-2