Linked Life Data

15126582

Source:http://linkedlifedata.com/resource/pubmed/id/15126582

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-5-5
pubmed:abstractText
Mifepristone in daily low doses has contraceptive potential by inhibiting ovulation. Follicular development is maintained, and although the endometrium is exposed to unopposed estrogen, there are no signs of hyperplasia or atypia. The mechanism of this antiestrogenic action is unknown. We have investigated the effect of daily low-dose mifepristone on proliferation markers and steroid receptors in surface epithelium, glands, and stroma of the endometrium. Endometrial biopsies were collected from 16 women before (late proliferative) and 60 and 120 d after taking 2 or 5 mg mifepristone daily for 120 d. Endometrial proliferation (H3 mitosis marker) and steroid (estrogen, progesterone, and androgen) receptor content were studied using standard immunocyotchemistry techniques. There was a significant decrease in the expression of H3 mitosis marker (P <or= 0.001) and progesterone receptor (P < 0.05) in endometrial glands and stroma by d 60 of treatment. In contrast, the expression of androgen receptor increased (P < 0.01) in glands, surface epithelium, and stroma compared with the pretreatment sample. These changes were maintained at 120 d of treatment. The expression of estrogen receptor was unchanged in stroma and surface epithelium; however, there was a significant decrease in expression after 120 d of treatment (P = 0.034). As androgens can antagonize estrogen action, enhanced glandular androgen receptor expression induced by mifepristone could play a role in its antiproliferative effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2491-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15126582-Adult, pubmed-meshheading:15126582-Biological Markers, pubmed-meshheading:15126582-Cell Division, pubmed-meshheading:15126582-Contraceptives, Oral, Synthetic, pubmed-meshheading:15126582-Dose-Response Relationship, Drug, pubmed-meshheading:15126582-Endometrium, pubmed-meshheading:15126582-Female, pubmed-meshheading:15126582-Histones, pubmed-meshheading:15126582-Hormone Antagonists, pubmed-meshheading:15126582-Humans, pubmed-meshheading:15126582-Mifepristone, pubmed-meshheading:15126582-Mitosis, pubmed-meshheading:15126582-Phosphorylation, pubmed-meshheading:15126582-Receptors, Androgen, pubmed-meshheading:15126582-Receptors, Estrogen, pubmed-meshheading:15126582-Receptors, Progesterone, pubmed-meshheading:15126582-Time Factors, pubmed-meshheading:15126582-Up-Regulation
pubmed:year
2004
pubmed:articleTitle
Low-dose mifepristone inhibits endometrial proliferation and up-regulates androgen receptor.
pubmed:affiliation
Contraceptive Development Network, Center for Reproductive Biology, Edinburgh, United Kingdom EH16 4SB.
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial, Research Support, Non-U.S. Gov't