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  • 자궁근종에서 타목시펜의 수용체를 통한 기전
  • The Action Mechanism of Tamoxifen Via Estrogen Receptor on Uterine Leimyoma
저자명
이병석,차동현,정경아,이희대,박기현,조동제,송찬호,Lee. Byung-Seok,Cha. Dong-Hyun,Jung. Kyung-Ah,Lee. Hye-Dae,Park. Ki-Hyun,Cho. Dong-Jae,Song. Chan-Ho
간행물명
대한불임학회지
권/호정보
2002년|29권 4호|pp.337-343 (7 pages)
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Objectives: To investigate the distribution of $ER{alpha}$, $ER{eta}$, c-fos and c-jun in the uterine myoma and myometrium in oder to know how the tamoxifen cause the growth of myoma. Methods: Myoma and myometrial tissue were obtained from the postmenopausal women treated with tamoxifen in the patients with breast cancer and in the premenopausal patients, who were undergoing myoma of uterus from 1998 through 2000. The espression of each gene was quantitated with quantitative RT-PCR. Results: The expression of $ER{alpha}$ was slightly increased in the myoma than the myometrium in the proliferative phase, and was slightly decreased in the myometrium than the myoma in the secretory phase. However it was not significant statistically. In the postmemopausal women treated with tamoxifen, $ER{alpha}$ was expressed in all myoma and myome1rial tissues and the expression was not statistically significant. The expression ofER~ was slightly increased in the myome1rium than the leiomyoma in the proliferative and secretory phase, but it was not significant statistically. In the postmemopausal women treated with tamoxifen, the expression of ER~ was significantly incresed in the myome1rium than the leiomyoma. The expression of c-fos was significantly increased in the myome1rium than the leiomyoma in the proliferative and secretory phase. In the postmemopausal women treated with tamoxifen, the expression of c-fos was slightly increased in the leiomyoma than the myomelrium, however, it was not statistically significant. Conclusion: Tamoxifen may cause the growth of leiomyoma by $ER{alpha}$ with AP-l pathway reducing the counteraction of 6$ER{eta}$ to $ER{alpha}$.