Cyclooxygenase as a target for chemoprevention in colorectal cancer: lost cause or a concept coming of age?
Affiliation
Beaumont Hospital, Department of Gastroenterology, Beaumont Road, Dublin, D8, Ireland. glen_doherty@hotmail.comIssue Date
2009-02MeSH
AnimalsAnti-Inflammatory Agents, Non-Steroidal
Anticarcinogenic Agents
Clinical Trials as Topic
Colorectal Neoplasms
Cyclooxygenase 2
Cyclooxygenase Inhibitors
Disease Models, Animal
Drug Delivery Systems
Humans
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Cyclooxygenase as a target for chemoprevention in colorectal cancer: lost cause or a concept coming of age? 2009, 13 (2):209-18 Expert Opin. Ther. TargetsJournal
Expert opinion on therapeutic targetsDOI
10.1517/14728220802653631PubMed ID
19236238Abstract
COX-2 is upregulated at an early stage in colorectal carcinogenesis and generates prostaglandins, which promote cancer cell proliferation, impair apoptosis and enhance angiogenesis, promoting tumour growth and metastasis. There are ample data from animal models and human studies to demonstrate enhanced tumour progression associated with COX-2 activity in cancer cells. Conversely, NSAIDs including aspirin inhibit COX-2 and, therefore, have anti-neoplastic properties. There has been sustained interest in COX-2 as a chemopreventive target in colorectal cancer (CRC) and although both aspirin and COX-2 selective NSAIDs have demonstrated efficacy, adverse effects have limited their widespread adoption. In particular, evidence of the cardiovascular effects of COX-2 selective inhibitors has led to questioning of the suitability of COX-2 as a target for chemoprevention. This review examines the basis for targeting COX-2 in CRC chemoprevention, evaluates the efficacy and safety of the approach and examines future strategies in this area.Item Type
ArticleLanguage
enISSN
1744-7631ae974a485f413a2113503eed53cd6c53
10.1517/14728220802653631
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