|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0007102,
umls-concept:C0007608,
umls-concept:C0009429,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0034802,
umls-concept:C0040624,
umls-concept:C0215737,
umls-concept:C0332206,
umls-concept:C0334227,
umls-concept:C0547047,
umls-concept:C0556895,
umls-concept:C1565860,
umls-concept:C1705323
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|
pubmed:issue |
5
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|
pubmed:dateCreated |
2007-9-19
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|
pubmed:abstractText |
The use of non-steroidal anti-inflammatory drugs has proved of great interest in the prevention and treatment of colorectal cancer, although their precise mechanisms of action remain unclear. Overexpression of cyclooxygenase-2 (COX-2) and subsequent prostaglandin production promote metastasis and have been shown to increase cell motility in vitro.
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pubmed:language |
eng
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pubmed:journal |
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|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
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pubmed:month |
Oct
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|
pubmed:issn |
0960-7722
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|
pubmed:author |
|
|
pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
768-79
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17877615-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:17877615-Base Sequence,
pubmed-meshheading:17877615-Cell Line, Tumor,
pubmed-meshheading:17877615-Cell Movement,
pubmed-meshheading:17877615-Colonic Neoplasms,
pubmed-meshheading:17877615-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:17877615-DNA Primers,
pubmed-meshheading:17877615-Dinoprostone,
pubmed-meshheading:17877615-Humans,
pubmed-meshheading:17877615-Nitrobenzenes,
pubmed-meshheading:17877615-Phosphorylation,
pubmed-meshheading:17877615-Receptor, Epidermal Growth Factor,
pubmed-meshheading:17877615-Sulfonamides,
pubmed-meshheading:17877615-Transcriptional Activation
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|
pubmed:year |
2007
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|
pubmed:articleTitle |
Inhibition of COX-2 with NS-398 decreases colon cancer cell motility through blocking epidermal growth factor receptor transactivation: possibilities for combination therapy.
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pubmed:affiliation |
Division of Histopathology, Department of Cellular and Molecular Medicine, School of Medical Sciences and Bristol Royal Infirmary, University of Bristol, Bristol, UK.
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pubmed:publicationType |
Journal Article
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