ArticleMolecular cytogenetics2015
A rare coincidence of different types of driver mutations among uterine leiomyomas (UL).
Article in Molecular cytogenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Prevalence and clinical significance of co-existing mutations inFrontiers in reproductive health · 2023Article
- Development of Primary Monolayer Cell Model and Organotypic Model of Uterine Leiomyoma.Methods and protocols · 2022Article
- Cytogenomic Profile of Uterine Leiomyoma: In Vivo vs. In Vitro Comparison.Biomedicines · 2021Article
- Molecular and Cellular Insights into the Development of Uterine Fibroids.International journal of molecular sciences · 2021Review
- Understanding Obesity as a Risk Factor for Uterine Tumors Using Drosophila.Advances in experimental medicine and biology · 2019Review
- Clinical, pathologic, cytogenetic, and molecular profiling in self-identified black women with uterine leiomyomata.Cancer genetics · 2018Article
- Genetic heterogeneity in leiomyomas of deep soft tissue.Oncotarget · 2017Article
- Factors affecting the loss of MED12-mutated leiomyoma cells during in vitro growth.Oncotarget · 2017Article
- Reasons to Reconsider Risk Associated With Power Morcellation of Uterine Fibroids.In vivo (Athens, Greece)Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of mediator subcomplex 12 (MED12) and of high mobility group protein AT-hook 2 (HMGA2) are driver mutations in uterine leiomyomas (UL) that have not been observed to coexist in one tumor and even rarely coexist in different UL tumors of one patient. Here we describe a patient who underwent hysterectomy because of multiple leiomyomas which were studied by cytogenetics, MED12 hotspot sequencing, and copy number variation arrays. Two of the UL tumors had different HMGA2 rearrangements not detected by G-banding. Two UL tumors had deletions of the long arm of chromosome 3, in one case associated with a MED12 mutation. Both deletions lead to the loss of MED12L showing strong similarity with MED12. It remains to be determined if this gene can play a role in leiomyomagenesis independent of MED12. In summary, the patient presented exhibits an unusual coincidence of different driver mutations among her leiomyomas.
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