Linked Life Data

9852399

Source:http://linkedlifedata.com/resource/pubmed/id/9852399

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-2-4
pubmed:abstractText
The critical mechanisms responsible for antiestrogen resistance have not yet been elucidated. We previously established a breast cancer cell line, KPL-1, derived from a patient with recurrent disease which appeared under tamoxifenadministration. In a previous study, we suggested that this cell line is estrogen receptor (ER)-positive but tamoxifen-resistant. In the present study, the effects of a pure antiestrogen, ICI 182,780, on this cell line were investigated. Although tamoxifen inhibited neither cell growth nor estradiol-stimulated transcriptional activity in vitro, ICI 182,780, significantly inhibited both of them. Tamoxifen and ICI 182,780 were then administered to female nude mice bearing KPL-1 tumors. Tamoxifen had no effect on tumor growth, but ICI 182,780 unexpectedly stimulated it (p = 0.022). Estradiol tended to inhibit tumor growth (p = 0.198). Immunohistochemical analysis revealed that ICI 182,780 significantly increased the Ki6-labeling index (p<0.001) but estradiol decreased it (p = 0.035). To explore the possible mechanisms of these phenotypes, the mRNA levels of ER-alpha,ER-beta, transforming growth factor-beta1, fibroblast growth factor (FGF)-1 and FGF-4 in KPL-1 cells were compared with those in other ER-positive human breast cancer cell lines by reverse-transcription polymerase chain reaction. FGF-1 was overexpressed only in KPL-1 cells. This cell line is the first breast cancer cell line to be growth-stimulated by ICI 182,780 in vivo. Paracrine interaction between tumor cells and stromal cells mediated by growth factors, such as FGF-1, might be a key factor to explain the unique hormone responsiveness of KPL-1 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0030-2414
pubmed:author
pubmed:issnType
Print
pubmed:volume
55 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9852399-Animals, pubmed-meshheading:9852399-Antineoplastic Agents, Hormonal, pubmed-meshheading:9852399-Breast Neoplasms, pubmed-meshheading:9852399-DNA Primers, pubmed-meshheading:9852399-Drug Resistance, Neoplasm, pubmed-meshheading:9852399-Estradiol, pubmed-meshheading:9852399-Estrogen Antagonists, pubmed-meshheading:9852399-Female, pubmed-meshheading:9852399-Fibroblast Growth Factors, pubmed-meshheading:9852399-Gene Expression Regulation, Neoplastic, pubmed-meshheading:9852399-Humans, pubmed-meshheading:9852399-Mice, pubmed-meshheading:9852399-Mice, Nude, pubmed-meshheading:9852399-Neoplasms, Hormone-Dependent, pubmed-meshheading:9852399-RNA, Messenger, pubmed-meshheading:9852399-RNA, Neoplasm, pubmed-meshheading:9852399-Receptors, Estrogen, pubmed-meshheading:9852399-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:9852399-Tamoxifen, pubmed-meshheading:9852399-Transforming Growth Factor beta, pubmed-meshheading:9852399-Tumor Cells, Cultured, pubmed-meshheading:9852399-Up-Regulation
pubmed:year
1998
pubmed:articleTitle
A pure antiestrogen, ICI 182,780, stimulates the growth of tamoxifen-resistant KPL-1 human breast cancer cells in vivo but not in vitro.
pubmed:affiliation
Department of Breast and Thyroid Surgery, Okayama, Japan. kure@med.kawasaki-m.ac.jp
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't