There is strong evidence for an important role for increased COX (cyclo-oxygenase)-2 expression and PG (prostaglandin) E2 production in colorectal tumorigenesis. PGE2 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-steidal 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.
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August 2005
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Conference Article|
August 01 2005
Prospects in NSAID-derived chemoprevention of colorectal cancer
S. Chell;
S. Chell
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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H.A. Patsos;
H.A. Patsos
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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D. Qualtrough;
D. Qualtrough
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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A.M. H-Zadeh;
A.M. H-Zadeh
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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D.J. Hicks;
D.J. Hicks
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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A. Kaidi;
A. Kaidi
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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I.R. Witherden;
I.R. Witherden
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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A.C. Williams;
A.C. Williams
1Cancer Research UK, Colorectal Tumour Biology Group, Department of Pathology and Microbiology, Bristol University, Bristol BS8 1TD, U.K.
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C. Paraskeva
C. Paraskeva
1
1To whom correspondence should be addressed (email c.paraskeva@bristol.ac.uk).
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Publisher: Portland Press Ltd
Received:
April 01 2005
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2005 The Biochemical Society
2005
Biochem Soc Trans (2005) 33 (4): 667–671.
Article history
Received:
April 01 2005
Citation
S. Chell, H.A. Patsos, D. Qualtrough, A.M. H-Zadeh, D.J. Hicks, A. Kaidi, I.R. Witherden, A.C. Williams, C. Paraskeva; Prospects in NSAID-derived chemoprevention of colorectal cancer. Biochem Soc Trans 1 August 2005; 33 (4): 667–671. doi: https://doi.org/10.1042/BST0330667
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