| Autor: |
Chell S; Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, UK., Patsos HA, Qualtrough D, H-Zadeh AM, Hicks DJ, Kaidi A, Witherden IR, Williams AC, Paraskeva C |
| Jazyk: |
angličtina |
| Zdroj: |
Biochemical Society transactions [Biochem Soc Trans] 2005 Aug; Vol. 33 (Pt 4), pp. 667-71. |
| DOI: |
10.1042/BST0330667 |
| Abstrakt: |
There is strong evidence for an important role for increased COX (cyclo-oxygenase)-2 expression and PG (prostaglandin) E2 production in colorectal tumorigenesis. PGE(2) acts through four E-prostanoid receptors (EP1-4). COX-2 has therefore become a target for the potential chemoprevention and therapy of colorectal cancer. However, any therapeutic/preventive strategy has the potential to have an impact on physiological processes and hence result in side effects. General COX (COX-1 and -2) inhibition by traditional NSAIDs (non-steroidal anti-inflammatory drugs), such as aspirin, although chemopreventive, has some side effects, as do some conventional COX-2-selective NSAIDs. As PGE2 is thought to be the major PG species responsible for promoting colorectal tumorigenesis, research is being directed to a number of protein targets downstream of COX-2 that might allow the selective inhibition of the tumour-promoting activities of PGE2, while minimizing the associated adverse events. The PGE synthases and E-prostanoid receptors (EP1-4) have therefore recently attracted considerable interest as potential novel targets for the prevention/therapy of colorectal cancer. Selective (and possibly combinatorial) inhibition of the synthesis and signalling of those PGs most highly associated with colorectal tumorigenesis may have some advantages over COX-2-selective inhibitors. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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