Details

Autor(en) / Beteiligte

• Chell, S
• Patsos, H A
• Qualtrough, D
• H-Zadeh, A M
• Hicks, D J
• Kaidi, A
• Witherden, I R
• Williams, A C
• Paraskeva, C

Titel

Prospects in NSAID-derived chemoprevention of colorectal cancer

Ist Teil von

• Biochemical Society transactions, 2005-08, Vol.33 (Pt 4), p.667-671

Ort / Verlag

England

Erscheinungsjahr

2005

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.