Abstract
Chronic inflammation and cancer are closely associated in the intestine. Anti-inflammatory medication reduces intestinal neoplasia, while colorectal cancer incidence is increased in ulcerative colitis. Cyclooxygenases are key to both diseases, yet the molecular basis of the association remains incompletely understood. Two recent Cell (Greten et al., 2004; Rakoff-Nahoum et al., 2004) papers illuminate roles of Toll-like receptors and the NF-kappaB pathway in the control of epithelial homeostasis in health and disease.
MeSH terms
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Animals
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Bacteria / genetics
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Bacteria / metabolism
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Cell Survival / genetics
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / immunology
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Colitis, Ulcerative / enzymology
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Colitis, Ulcerative / immunology
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Colitis, Ulcerative / physiopathology*
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Cyclooxygenase 1
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Humans
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Intestinal Mucosa / enzymology
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Intestinal Mucosa / immunology
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Intestinal Mucosa / physiopathology*
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Intestinal Neoplasms / enzymology
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Intestinal Neoplasms / immunology
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Intestinal Neoplasms / physiopathology*
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Isoenzymes / metabolism
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / metabolism*
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Membrane Proteins
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NF-kappa B / genetics
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NF-kappa B / metabolism*
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Prostaglandin-Endoperoxide Synthases / metabolism
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / metabolism*
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Toll-Like Receptors
Substances
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Isoenzymes
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Membrane Glycoproteins
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Membrane Proteins
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NF-kappa B
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Receptors, Cell Surface
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Toll-Like Receptors
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Cyclooxygenase 1
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PTGS1 protein, human
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Prostaglandin-Endoperoxide Synthases