Literature DB >> 11163834

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

O Khorram1, M Garthwaite, E Grosen, T Golos.   

Abstract

OBJECTIVE: To determine uterine and ovarian expression of growth hormone-releasing hormone (GHRH) messenger RNA (mRNA) in benign and pathologic gynecologic states.
DESIGN: Case-control study.
SETTING: Tertiary-care academic department. PATIENT(S): Women undergoing hysterectomy for benign or malignant gynecologic 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 compared with those in tissues with pathologic abnormalities. RESULT(S): Growth hormone-releasing hormone mRNA was detectable in the ovary, endometrium, myometrium, fallopian tubes, and placenta. Levels of GHRH mRNA were significantly increased in secretory endometrium compared with proliferative endometrium. Hormone replacement therapy did not affect endometrial 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 noncancerous myometrial tissue obtained from other patients with benign gynecologic disease. In ovarian tissue, no differences in GHRH mRNA were found between premenopausal and postmenopausal women. Ovarian GHRH mRNA was significantly 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 factors as ovarian hormones. Because it is a growth factor, GHRH may promote endometrial proliferation and may be involved in the pathogenesis of ovarian and endometrial cancer and endometriosis.

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Year:  2001        PMID: 11163834     DOI: 10.1016/s0015-0282(00)01658-7

Source DB:  PubMed          Journal:  Fertil Steril        ISSN: 0015-0282            Impact factor:   7.329


  15 in total

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