Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-11-23
pubmed:abstractText
The identification of biomarkers in prostatic carcinoma has yielded important data regarding prognosis and has aided in increasing diagnostic accuracy. Additionally, this approach has yielded important insights into the biology of prostatic carcinoma. In this study, we report that the expression of the cyclooxygenase isoenzyme, COX-2, is significantly increased in prostatic carcinoma, whereas that of the cell adhesion molecule, E-cadherin, is decreased. The expression of COX-2 was positively correlated with higher tumor stage, and the presence of carcinoma in surgical margins at prostatectomy. Conversely, the expression of E-cadherin was inversely related to these prognostic indicators. Lastly, the expressions of COX-2 and E-cadherin were very strongly and inversely correlated. These results provide important insights into the biologic underpinnings of prostate carcinoma; and further studies into COX-2 expression in prostate core biopsies may show utility in preprostatectomy prognostication. Furthermore, these results may provide a rational basis for therapeutic intervention and chemoprevention with COX-2 inhibitor therapy in prostate carcinoma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1541-2016
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
375-83
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
An inverse relation between COX-2 and E-cadherin expression correlates with aggressive histologic features in prostate cancer.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, UCLA, Los Angeles, CA 90095, drao@mednet.ucla.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural