Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Med Sci. 2014 Jan 28;11(3):276-81. doi: 10.7150/ijms.7627. eCollection 2014.

Comparison of the inhibitory effect of gonadotropin releasing hormone (GnRH) agonist, selective estrogen receptor modulator (SERM), antiprogesterone on myoma cell proliferation in vitro.

Author information

1
1. Department of Obstetrics and Gynecology, The Catholic University of Korea, Republic of Korea.
2
2. Department of Hospital Pathology, The Catholic University of Korea, Republic of Korea.

Abstract

Uterine myomas are the most common gynecologic tumor in women of reproductive age. Treatment options of uterine myomas consist of surgical, medical and interventional therapy such as uterine artery embolization or myolysis. Given that it is the most common type of tumor in women of reproductive age, the treatment of uterine myomas must prioritize uterine conservation. There are several drugs for medical treatment of uterine myoma such as gonadotropin releasing hormone (GnRH) agonist, selective estrogen receptor modulator (SERM) and antiprogesterone. The objective of this study was to compare the effect of GnRH agonist, SERM, and antiprogesterone in the treatment of uterine myomas in vitro. The effect of drugs was evaluated through the cell viability assay in cultured leiomyoma cells, western blot analysis of proliferating cell nuclear antigen (PCNA), and BCL-2 protein expression. As a result, mifepristone single-treated group represents the most significant reduction in myoma cell viability and proliferation. When pretreated with leuprolide acetate, raloxifene shows more significant reduction in myoma cell viability and proliferation than mifepristone. This study suggests one of the possible mechanisms how medications act on uterine myoma, especially at the molecular level.

KEYWORDS:

Drug therapy; Gonadotropin-releasing hormone agonist; Leiomyoma; Mifepristone; Raloxifene

PMID:
24516352
PMCID:
PMC3917117
DOI:
10.7150/ijms.7627
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Ivyspring International Publisher Icon for PubMed Central
    Loading ...
    Support Center