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dc.contributor.authorDoherty, Glen A
dc.contributor.authorMurray, Frank E
dc.date.accessioned2011-04-07T08:53:28Z
dc.date.available2011-04-07T08:53:28Z
dc.date.issued2009-02
dc.identifier.citationCyclooxygenase as a target for chemoprevention in colorectal cancer: lost cause or a concept coming of age? 2009, 13 (2):209-18 Expert Opin. Ther. Targetsen
dc.identifier.issn1744-7631
dc.identifier.pmid19236238
dc.identifier.doi10.1517/14728220802653631
dc.identifier.urihttp://hdl.handle.net/10147/127645
dc.description.abstractCOX-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.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal
dc.subject.meshAnticarcinogenic Agents
dc.subject.meshClinical Trials as Topic
dc.subject.meshColorectal Neoplasms
dc.subject.meshCyclooxygenase 2
dc.subject.meshCyclooxygenase Inhibitors
dc.subject.meshDisease Models, Animal
dc.subject.meshDrug Delivery Systems
dc.subject.meshHumans
dc.titleCyclooxygenase as a target for chemoprevention in colorectal cancer: lost cause or a concept coming of age?en
dc.typeArticleen
dc.contributor.departmentBeaumont Hospital, Department of Gastroenterology, Beaumont Road, Dublin, D8, Ireland. glen_doherty@hotmail.comen
dc.identifier.journalExpert opinion on therapeutic targetsen
dc.description.provinceLeinster
html.description.abstractCOX-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.


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