Abstract
Uterine fibroids (UFs), benign myometrial tumors, negatively impact female reproductive health. The accepted model for their origin implicates somatic fibroid-causing mutations in gene MED12 (detected in ∼85% of all sporadic human UFs) in myometrial stem cells (MSCs) converting them into UF-forming MSCs. While the origin of these mutations remains unknown, defective DNA repair systems increase the risk of emergence of somatic tumor-forming mutations. We have shown earlier that Tsc2-mutant Eker (Tsc2Ek/+) rats exposed to diethylstilbestrol (DES, a tool compound of environmental EDCs) during early-life uterus development form fibroids at high frequency later in adult life versus unexposed counterparts.
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