Abstract
A model of immune evasion mediated by tumors expressing constitutively activated Stat3 was recently proposed in Nature Medicine by Wang et al., suggesting opportunities for a new therapeutic approach for cancer.
MeSH terms
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Cell Division
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Chemokine CCL5 / immunology
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Chemokine CCL5 / metabolism
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DNA-Binding Proteins / metabolism*
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Dendritic Cells / immunology*
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Dendritic Cells / metabolism
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Gene Expression Regulation, Neoplastic / immunology
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Gene Expression Regulation, Neoplastic / physiology
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Genes, MHC Class II / physiology*
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Interleukin-10 / immunology
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Interleukin-10 / metabolism
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Interleukin-6 / immunology
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Interleukin-6 / metabolism
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Models, Molecular
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Neoplasms / immunology
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Neoplasms / metabolism
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Phosphotyrosine
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STAT3 Transcription Factor
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Signal Transduction
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism
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Trans-Activators / metabolism*
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Tumor Necrosis Factor-alpha / immunology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Chemokine CCL5
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DNA-Binding Proteins
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Interleukin-6
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STAT3 Transcription Factor
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TNF protein, human
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Trans-Activators
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Tumor Necrosis Factor-alpha
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Interleukin-10
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Phosphotyrosine