Purpose of review
Uterine fibroids are extremely common, and can cause significant morbidity, yet the exact cause of these tumors remains elusive and there are currently no long-term treatments available. In this review, we aim to provide an overview of steroid hormones, genetic abnormalities, and stem cells in the pathogenesis of uterine fibroids.
A universal feature of fibroids is responsiveness to estrogen and progesterone, and most of the currently available therapies exploit this characteristic. Ulipristal acetate has recently shown particular promise for providing long-term relief from uterine fibroids. Additionally, fibroid stem cells were isolated and appear to be necessary for growth. The recent discovery of somatic mutations involving mediator subunit complex 12 (MED12) or high-mobility group AT-hook 2 (HMGA2) in the majority of fibroids and the links to their pathophysiology were also significant advances.
The recent shift in focus from hormones to fibroid stem cells and genetic aberrations should lead not only to a deeper understanding of the specific cause of fibroids, but also to the discovery of new therapeutic targets. Targeting the products of genetic mutations or fibroid stem cells has the potential to achieve both better control of current tumors and the prevention of new fibroids.