Abstract

Uterine leiomyomas (fibroids) represent the most common reproductive-age benign tumor in women. Two distinct subtypes, which carry a Mediator complex subunit 12 (MED12) mutation (mut-MED12) or with high mobility group AT-hook 2 (HMGA2) overexpression (ov-HMGA2), comprise 85% of all leiomyomas. A universal feature of all leiomyomas is responsiveness to estrogen and progesterone, which function by activating their cognate nuclear receptors ERα and PR, respectively, to increase their binding to regulatory regions of target genes and control their transcription and function.

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