Endocrine-disrupting chemicals and uterine fibroids

被引:49
|
作者
Katz, Tiffany A. [1 ]
Yang, Qiwei [2 ]
Trevino, Lindsey S. [1 ]
Walker, Cheryl Lyn [1 ]
Al-Hendy, Ayman [2 ]
机构
[1] Texas A&M Univ, Hlth Sci Ctr, Inst Biotechnol, Ctr Translat Canc Res, Houston, TX USA
[2] Augusta Univ, Dept Obstet & Gynecol, Med Coll Georgia, 1120 15th St, Augusta, GA 30912 USA
基金
美国国家卫生研究院;
关键词
Endocrine-disrupting chemicals; uterine fibroids; PROGESTERONE-RECEPTOR MODULATORS; RENAL-CELL CANCER; PRENATAL DIETHYLSTILBESTROL EXPOSURE; COUPLED ESTROGEN-RECEPTOR; FUMARATE-HYDRATASE GENE; TUMOR-INITIATING CELLS; MED12; EXON-2; MUTATIONS; MYOMETRIAL STEM-CELLS; SMOOTH-MUSCLE-CELLS; LEIOMYOMA CELLS;
D O I
10.1016/j.fertnstert.2016.08.023
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Uterine fibroids are the most frequent gynecologic tumor, affecting 70% to 80% of women over their lifetime. Although these tumors are benign, they can cause significant morbidity and may require invasive treatments such as myomectomy and hysterectomy. Many risk factors for these tumors have been identified, including environmental exposures to endocrine-disrupting chemicals (EDCs) such as genistein and diethylstilbestrol. Uterine development may be a particularly sensitive window to environmental exposures, as some perinatal EDC exposures have been shown to increase tumorigenesis in both rodent models and human epidemiologic studies. The mechanisms by which EDC exposures may increase tumorigenesis are still being elucidated, but epigenetic reprogramming of the developing uterus is an emerging hypothesis. Given the remarkably high incidence of uterine fibroids and their significant impact on women's health, understanding more about how prenatal exposures to EDCs (and other environmental agents) may increase fibroid risk could be key to developing prevention and treatment strategies in the future. (C) 2016 by American Society for Reproductive Medicine.
引用
收藏
页码:967 / 977
页数:11
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