Human uterine and ovarian expression of growth hormone-releasing hormone messenger RNA in benign and malignant gynecologic conditions

Citation
O. Khorram et al., Human uterine and ovarian expression of growth hormone-releasing hormone messenger RNA in benign and malignant gynecologic conditions, FERT STERIL, 75(1), 2001, pp. 174-179
Citations number
20
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
FERTILITY AND STERILITY
ISSN journal
00150282 → ACNP
Volume
75
Issue
1
Year of publication
2001
Pages
174 - 179
Database
ISI
SICI code
0015-0282(200101)75:1<174:HUAOEO>2.0.ZU;2-I
Abstract
Objective: To determine uterine and ovarian expression of growth hormone-re leasing hormone (GHRH) messenger RNA (mRNA) in benign and pathologic gyneco logic states. Design: Case-control study. Setting: Tertiary-care academic department. Patient(s): Women undergoing hysterectomy for benign or malignant gynecolog ic conditions. Intervention(s): Ovarian and uterine tissue was obtained for measurement of GHRH mRNA levels by reverse transcription polymerase chain reaction. Main Outcome Measure(s): Levels of GHRH mRNA in normal tissues were compare d with those in tissues with pathologic abnormalities. Result(s): Growth hormone-releasing hormone mRNA was detectable in the ovar y, endometrium, myometrium, fallopian tubes, and placenta. Levels of GHRH m RNA were significantly increased in secretory endometrium compared with pro liferative endometrium. Hormone replacement therapy did not affect endometr ial GHRH mRNA levels. Uterine myomas expressed similar levels of GHRH mRNA as normal myometrium. No changes in endometrial GHRH mRNA were detected in endometrial cancers compared with normal endometrium or myometrium obtained from the same patient; however, these levels were higher than those in non cancerous myometrial tissue obtained from other patients with benign gyneco logic disease. In ovarian tissue, no differences in GHRH mRNA were found be tween premenopausal and postmenopausal women. Ovarian GHRH mRNA was signifi cantly decreased in endometriotic cysts, whereas significantly greater GHRH expression occurred in ovarian cancer compared with normal ovarian tissue. Conclusion(s): Endometrial and ovarian GHRH gene transcription are altered in selective physiologic and pathologic states and are influenced by such f actors as ovarian hormones, Because it is a growth factor, GHRH may promote endometrial proliferation and may be involved in the pathogenesis of ovari an and endometrial cancer and endometriosis. (C) 2001 by American Society f or Reproductive Medicine.