Linked Life Data

12066205

Source:http://linkedlifedata.com/resource/pubmed/id/12066205

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-6-14
pubmed:abstractText
Cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF) have been reported to be significantly related to carcinogenesis or progression of various cancers. However, there has been no report on the relation between COX-2 and VEGF overexpression in pancreatic tumors. We investigated the overexpression of COX-2 and VEGF immunohistochemically in intraductal papillary-mucinous tumors (IPMT) and invasive ductal carcinoma (IDC) and examined the relationship with clinicopathological factors and the correlation between these immunoactivities in IPMT and IDC. In IPMT, the positive rates of COX-2 overexpression were 0% in 10 areas of hyperplasia, 54.5% of adenoma, 83.3% of intraductal areas of adenocarcinoma, and 66.7% of invasive areas of adenocarcinoma. On the contrary, 47.8% of IDC were positive for COX-2 overexpression. The positive rates of VEGF in IPMT were 10% in areas of hyperplasia, 54.5% of adenoma, 66.7% of intraductal areas of adenocarcinoma and 66.7% of invasive areas of adenocarcinoma. However, in IDC it was 47.8%. Only lymph node metastasis correlated significantly with VEGF overexpression (p=0.04), while the other factors had no significant relationships with either COX-2 or VEGF overexpression. There was a statistically significant correlation between COX-2 and VEGF overexpression in IPMT (p<0.001), in 5 patients with adenoma of which both COX-2 and VEGF were stained in almost exactly the same locations. On the contrary, COX-2 and VEGF overexpression had no statistically significant relationship in IDC. In conclusion, we demonstrate evidence of COX-2 and VEGF overexpression in human pancreatic tumors. Chemoprevention via the suppression of angiogenesis by means of COX-2 inhibitor may be more effective in IPMT than in IDC, because of the strong correlation of both factors especially in IPMT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1021-335X
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
761-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12066205-Adenocarcinoma, pubmed-meshheading:12066205-Adenocarcinoma, Mucinous, pubmed-meshheading:12066205-Adenoma, pubmed-meshheading:12066205-Carcinoma, Pancreatic Ductal, pubmed-meshheading:12066205-Cyclooxygenase 2, pubmed-meshheading:12066205-Endothelial Growth Factors, pubmed-meshheading:12066205-Humans, pubmed-meshheading:12066205-Immunoenzyme Techniques, pubmed-meshheading:12066205-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12066205-Isoenzymes, pubmed-meshheading:12066205-Lymphatic Metastasis, pubmed-meshheading:12066205-Lymphokines, pubmed-meshheading:12066205-Membrane Proteins, pubmed-meshheading:12066205-Neoplasm Invasiveness, pubmed-meshheading:12066205-Pancreatic Neoplasms, pubmed-meshheading:12066205-Papilloma, Intraductal, pubmed-meshheading:12066205-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:12066205-Vascular Endothelial Growth Factor A, pubmed-meshheading:12066205-Vascular Endothelial Growth Factors
pubmed:articleTitle
Expression of cyclooxygenase-2 and vascular endothelial growth factor in pancreatic tumors.
pubmed:affiliation
Department of Surgery, Tokyo Medical University, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't