Linked Life Data

12684660

Source:http://linkedlifedata.com/resource/pubmed/id/12684660

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-4-9
pubmed:abstractText
Metastasis or progression of ovarian cancer cells is known to be due to the action of various angiogenic factors. We determined the expression of thymidine phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) and vascular endothelial growth factor (VEGF) in cell lines established from 3 serous adenocarcinomas, 3 clear cell carcinomas and 2 mucinous carcinomas of the human ovary. TP activity and the TP mRNA level were much higher in the serous adenocarcinoma cells than in the clear cells and mucinous carcinoma cells, and TP expression was extremely low in the clear cell carcinoma cells. Expression of VEGF mRNA was variable, but not significantly different between the 3 histological types of ovarian cancer. In vivo angiogenesis in the ovarian cancer cells was evaluated by the dorsal air sac assay and revealed that SHIN-3 and HRA serous adenocarcinoma cells, which have high levels of TP expression, induced angiogenesis, while KK clear cell carcinoma cells with low TP expression, did not. The degree of ovarian-cancer-induced angiogenesis seemed to be independent of expression of VEGF in the cells. To confirm that the serous adenocarcinoma-induced angiogenesis is dependent on TP levels, a potent and specific inhibitor of TP was administered orally to mice implanted with a chamber containing SHIN-3 or HRA cells. The TP inhibitor significantly inhibited the angiogenesis induced by the serous adenocarcinoma cells. These results suggest that the angiogenic potency of ovarian cancer cells differs with the histological type and is controlled by expression of TP/PD-ECGF, not by VEGF, and that TP-mediated angiogenesis may be the main factor responsible for progression or metastasis of ovarian serous adenocarcinomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1019-6439
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
961-7
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed-meshheading:12684660-Adenocarcinoma, Clear Cell, pubmed-meshheading:12684660-Adenocarcinoma, Mucinous, pubmed-meshheading:12684660-Animals, pubmed-meshheading:12684660-Base Sequence, pubmed-meshheading:12684660-Cystadenocarcinoma, Serous, pubmed-meshheading:12684660-DNA Primers, pubmed-meshheading:12684660-Endothelial Growth Factors, pubmed-meshheading:12684660-Enzyme Inhibitors, pubmed-meshheading:12684660-Female, pubmed-meshheading:12684660-Gene Expression Regulation, Neoplastic, pubmed-meshheading:12684660-Humans, pubmed-meshheading:12684660-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12684660-Lymphokines, pubmed-meshheading:12684660-Mice, pubmed-meshheading:12684660-Neovascularization, Pathologic, pubmed-meshheading:12684660-Ovarian Neoplasms, pubmed-meshheading:12684660-Polymerase Chain Reaction, pubmed-meshheading:12684660-Thymidine Phosphorylase, pubmed-meshheading:12684660-Transplantation, Heterologous, pubmed-meshheading:12684660-Tumor Cells, Cultured, pubmed-meshheading:12684660-Vascular Endothelial Growth Factor A, pubmed-meshheading:12684660-Vascular Endothelial Growth Factors
pubmed:year
2003
pubmed:articleTitle
Thymidine phosphorylase-mediated angiogenesis regulated by thymidine phosphorylase inhibitor in human ovarian cancer cells in vivo.
pubmed:affiliation
Jichi Medical School, Tochigi 329-0498, Japan.
pubmed:publicationType
Journal Article