Uterine Fibroids: From Molecular Basis to Therapy
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 12446
Special Issue Editor
Interests: uterine fibroids; reproductive surgery; uterine biology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Uterine fibroids are the most frequent pelvic neoplasms and occur in about 20–30% of women of childbearing age, with a peak of 70% of women around the age of 45. Although many fibroids are asymptomatic and of small size, about 50% of women that develop symptomatic fibroids require medical intervention, with a significantly higher incidence in black women. Where drug treatment fails to improve symptoms satisfactorily, surgical removal of the fibroid remains the preferred approach. Despite the widely demonstrated effects of sex steroids on the growth of fibroids, the etiopathogenesis of uterine fibromatosis remains partially uncharacterized. In particular, the role of estrogen and progesterone is crucial not only for the understanding of the pathogenesis, but also for the treatment of the fibroids themselves. In fact, the receptors of these two hormones have increased expression in fibroids compared to healthy tissue. In addition to the cytological aspect, increased expression of estrogen and progesterone receptors was reported in immunohistochemical tests on tissue, and this was correlated with increased growth rate of the fibroid. Progesterone, like estrogen, also appears to play an etiopathogenetic role in uterine fibromatosis. Keeping in mind recent evidence reporting that estrogens increase the expression of progesterone receptors, there is also some evidence reported for the de novo synthesis of estrogen by fibroid cells. This autocrine production seems to be due to overexpression of the aromatase enzyme, which converts androgens into estrogens. It has, in fact, been shown that there is an accumulation of estradiol within myoma cells, which leads to an overregulation of estrogen receptors with consequent hypersensitivity to this hormone. This process results in overexpression of the progesterone receptor and its responsiveness, with a consequent increase in cell proliferation. Moreover, uterine fibroids are monoclonal neoplasms originating from mutation of a myocyte. In this regard, about 50% of uterine fibroids have chromosomal aberrations. The defect that is most encountered is the mutual translocation of chromosomes 12q15 and 14q24 at the level of the HMGIC gene, on chromosome 12, encoding the protein transcription factor HMGIC.
This Special Issue wishes to focus on basic and translational research, as well as molecular and hormonal evidence, toward obtaining a more complete comprehension of the etiopathology and pathophysiology of uterine fibroids and its translation into current clinical and gynecological practices for fibroid treatment.
Prof. Dr. Andrea Tinelli
Guest Editor
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Keywords
- uterine fibroids
- uterine myoma
- leiomyoma
- reproduction
- pregnancy
- GnRH agonists
- exogenous progestogens
- antiprogestens
- selective modulators of progesterone receptors
- tranexamic acid
- non-steroidal anti-inflammatory drugs
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