Linked Life Data

18508998

Source:http://linkedlifedata.com/resource/pubmed/id/18508998

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-5-29
pubmed:abstractText
The estrogen pathway plays an important role in the etiology of human endometrial carcinoma (EC). We examined whether estrogen biosynthesis in the tumor microenvironment promotes endometrial cancer. To examine the contribution of stromal cells to estrogen signaling in EC, we used reporter cells stably transfected with the estrogen response element (ERE) fused to the destabilized green fluorescent protein (GFP) gene. In this system, the endometrial cancer stromal cells from several patients activated the ERE of cancer cells to a variable extent. The GFP expression level increased when testosterone, a substrate for aromatase, was added. The effect was variably inhibited by aromatase inhibitors (AIs), although the response to AIs varied among patients. These results suggest that GFP expression is driven by estrogen synthesized by aromatase in the endometrial cancer stromal cells. In a second experiment, we constructed an adenovirus reporter vector containing the same construct as the reporter cells described above, and visualized endogenous ERE activity in primary culture cancer cells from 15 EC specimens. The GFP expression levels varied among the cases, and in most primary tissues, ERE activities were strongly inhibited by a pure anti-estrogen, fulvestrant. Interestingly, a minority of primary tissues in endometrial cancer showed ERE activity independent of the estrogen-ER pathway. These results suggest that AI may have some therapeutic value in EC; however, the hormonal microenvironment must be assessed prior to initiating therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1351-0088
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
451-63
pubmed:meshHeading
pubmed-meshheading:18508998-17-Hydroxysteroid Dehydrogenases, pubmed-meshheading:18508998-Adenoviridae, pubmed-meshheading:18508998-Aromatase, pubmed-meshheading:18508998-Aromatase Inhibitors, pubmed-meshheading:18508998-Breast Neoplasms, pubmed-meshheading:18508998-Cell Communication, pubmed-meshheading:18508998-Cell Line, Tumor, pubmed-meshheading:18508998-Endometrial Neoplasms, pubmed-meshheading:18508998-Estrogens, pubmed-meshheading:18508998-Female, pubmed-meshheading:18508998-Genes, Reporter, pubmed-meshheading:18508998-Green Fluorescent Proteins, pubmed-meshheading:18508998-Humans, pubmed-meshheading:18508998-Middle Aged, pubmed-meshheading:18508998-Receptors, Estrogen, pubmed-meshheading:18508998-Signal Transduction, pubmed-meshheading:18508998-Stromal Cells, pubmed-meshheading:18508998-Testosterone
pubmed:year
2008
pubmed:articleTitle
Estrogen signaling ability in human endometrial cancer through the cancer-stromal interaction.
pubmed:affiliation
Department of Medical Technology, Tohoku University School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai 981-0872, Japan. m-matsumoto@mail.tains.tohoku.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't