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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 9631

Special Issue Editor

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

Published Papers (2 papers)

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16 pages, 5482 KiB  
Article
Transcriptome Analyses of Myometrium from Fibroid Patients Reveals Phenotypic Differences Compared to Non-Diseased Myometrium
by Emmanuel N. Paul, Gregory W. Burns, Tyler J. Carpenter, Joshua A. Grey, Asgerally T. Fazleabas and Jose M. Teixeira
Int. J. Mol. Sci. 2021, 22(7), 3618; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073618 - 31 Mar 2021
Cited by 11 | Viewed by 2350
Abstract
Uterine fibroid tissues are often compared to their matched myometrium in an effort to understand their pathophysiology, but it is not clear whether the myometria of uterine fibroid patients represent truly non-disease control tissues. We analyzed the transcriptomes of myometrial samples from non-fibroid [...] Read more.
Uterine fibroid tissues are often compared to their matched myometrium in an effort to understand their pathophysiology, but it is not clear whether the myometria of uterine fibroid patients represent truly non-disease control tissues. We analyzed the transcriptomes of myometrial samples from non-fibroid patients (M) and compared them with fibroid (F) and matched myometrial (MF) samples to determine whether there is a phenotypic difference between fibroid and non-fibroid myometria. Multidimensional scaling plots revealed that M samples clustered separately from both MF and F samples. A total of 1169 differentially expressed genes (DEGs) (false discovery rate < 0.05) were observed in the MF comparison with M. Overrepresented Gene Ontology terms showed a high concordance of upregulated gene sets in MF compared to M, particularly extracellular matrix and structure organization. Gene set enrichment analyses showed that the leading-edge genes from the TGFβ signaling and inflammatory response gene sets were significantly enriched in MF. Overall comparison of the three tissues by three-dimensional principal component analyses showed that M, MF, and F samples clustered separately from each other and that a total of 732 DEGs from F vs. M were not found in the F vs. MF, which are likely understudied in the pathogenesis of uterine fibroids and could be key genes for future investigation. These results suggest that the transcriptome of fibroid-associated myometrium is different from that of non-diseased myometrium and that fibroid studies should consider using both matched myometrium and non-diseased myometrium as controls. Full article
(This article belongs to the Special Issue Uterine Fibroids: From Molecular Basis to Therapy)
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Review

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21 pages, 22348 KiB  
Review
Molecular and Cellular Insights into the Development of Uterine Fibroids
by Alba Machado-Lopez, Carlos Simón and Aymara Mas
Int. J. Mol. Sci. 2021, 22(16), 8483; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168483 - 06 Aug 2021
Cited by 36 | Viewed by 6466
Abstract
Uterine leiomyomas represent the most common benign gynecologic tumor. These hormone-dependent smooth-muscle formations occur with an estimated prevalence of ~70% among women of reproductive age and cause symptoms including pain, abnormal uterine bleeding, infertility, and recurrent abortion. Despite the prevalence and public health [...] Read more.
Uterine leiomyomas represent the most common benign gynecologic tumor. These hormone-dependent smooth-muscle formations occur with an estimated prevalence of ~70% among women of reproductive age and cause symptoms including pain, abnormal uterine bleeding, infertility, and recurrent abortion. Despite the prevalence and public health impact of uterine leiomyomas, available treatments remain limited. Among the potential causes of leiomyomas, early hormonal exposure during periods of development may result in developmental reprogramming via epigenetic changes that persist in adulthood, leading to disease onset or progression. Recent developments in unbiased high-throughput sequencing technology enable powerful approaches to detect driver mutations, yielding new insights into the genomic instability of leiomyomas. Current data also suggest that each leiomyoma originates from the clonal expansion of a single transformed somatic stem cell of the myometrium. In this review, we propose an integrated cellular and molecular view of the origins of leiomyomas, as well as paradigm-shifting studies that will lead to better understanding and the future development of non-surgical treatments for these highly frequent tumors. Full article
(This article belongs to the Special Issue Uterine Fibroids: From Molecular Basis to Therapy)
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