Linked Life Data

12885487

Source:http://linkedlifedata.com/resource/pubmed/id/12885487

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9379
pubmed:dateCreated
2003-7-29
pubmed:abstractText
CONTEXT: Colorectal cancer is the second most common cause of cancer-related mortality in the west. The high incidence and mortality make effective prevention an important public-health and economic issue. Non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit colorectal carcinogenesis and are among the few agents known to be chemopreventive. Randomised trials have shown that sulindac and celecoxib suppress the development of adenomatous polyps and cause regression of existing polyps in patients with familial adenomatous polyposis (FAP), who have a high risk for developing colorectal cancer. The mechanisms by which NSAIDs inhibit neoplastic growth are not fully known. STARTING POINT: Two recently reported randomised placebo-controlled trials show a chemopreventive effect of aspirin in populations other than those with FAP (Robert Sandler and colleagues, N Engl J Med 2003; 348: 883-90; John Baron and colleagues, N Engl J Med 2003; 348: 891-99). In the Sandler study 635 patients with colorectal cancer were randomised to receive 325 mg aspirin or placebo daily. After a follow-up of around 31 months, the mean number of adenomas was lower in the aspirin group than in the placebo group, corresponding to a relative risk of any recurrent adenoma in the aspirin group of 0.65. In the Baron study 1121 patients with colorectal adenomas were assigned to receive 81 or 325 mg aspirin or placebo daily. Follow-up colonoscopy, 32 months after the index endoscopy, showed an incidence of one or more adenomas of 38% in the 81 mg aspirin group, 45% in the 325 mg aspirin group, and 47% in the placebo group. Together, these studies indicate a moderate chemopreventive effect of aspirin in populations with an intermediate risk of developing colorectal cancer. WHERE NEXT? The anticancer properties of NSAIDs have been demonstrated in vitro and in animal studies, epidemiological reports, and intervention studies. Several mechanisms through which NSAIDs alter colonic carcinogenesis have been elucidated, including the induction of apoptosis in neoplastic cells, via mechanisms dependent and independent of cyclo-oxygenase. Some studies have suggested an important role for the cell-cycle regulating protein p21 in mediating the chemopreventive effect of sulindac. A decrease in p21 expression may be one of the main oncogenic events in the development of colorectal cancer. Thus p21 could be the molecular link in the chemopreventive effects of NSAIDs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1474-547X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
362
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
230-2
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Non-steroidal anti-inflammatory drugs and molecular carcinogenesis of colorectal carcinomas.
pubmed:affiliation
Department of Internal Medicine, University Hospital Groningen, Groningen, Netherlands. g.huls@int.azg.nl <g.huls@int.azg.nl>
pubmed:publicationType
Journal Article, Review