Abstract
Two inflammatory cytokines, IL-23 and IL-17A, produced by myeloid cells and different lymphocyte subsets, were found to play important pathogenic functions in several inflammation-related cancers. In colorectal cancer, elevated expression of IL-23, IL-23 receptor and IL-17A has been linked to adverse prognostic outcome and rapid progression to metastatic disease. In mouse models of colorectal tumourigenesis genetic or pharmacological inhibition of these cytokines attenuates tumour development and malignant progression. Collectively, such findings suggest that IL-23 and/or IL-17A inhibitors should be evaluated for their therapeutic and preventative potential in human cancers, especially in colorectal cancer.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology
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Anticarcinogenic Agents / pharmacology
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / immunology*
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Cell Transformation, Neoplastic / metabolism
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Cell Transformation, Neoplastic / pathology
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Colorectal Neoplasms / genetics
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Colorectal Neoplasms / immunology*
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Colorectal Neoplasms / metabolism
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Colorectal Neoplasms / pathology
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Colorectal Neoplasms / prevention & control
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Disease Models, Animal
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Humans
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Inflammation / drug therapy
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Inflammation / genetics
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Inflammation / immunology*
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Inflammation / metabolism
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Inflammation Mediators / antagonists & inhibitors
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Inflammation Mediators / immunology*
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Inflammation Mediators / metabolism
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Interleukin-17 / antagonists & inhibitors
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Interleukin-17 / genetics
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Interleukin-17 / immunology*
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Interleukin-17 / metabolism
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Interleukin-23 / antagonists & inhibitors
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Interleukin-23 / genetics
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Interleukin-23 / immunology*
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Interleukin-23 / metabolism
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Mice
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Signal Transduction* / drug effects
Substances
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Anti-Inflammatory Agents
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Anticarcinogenic Agents
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Inflammation Mediators
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Interleukin-17
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Interleukin-23