ArticleIn vivo (Athens, Greece)
Fusion of the
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The estrogen-progestogen-oxidative stress network in uterine fibroids: mechanistic insights and therapeutic opportunities.Redox report : communications in free radical research · 2026Review
- Clinical prognostic value of imaging and immuno-hormonal markers in uterine leiomyoma.Quantitative imaging in medicine and surgery · 2026Article
- High mobility group protein 2 (HMGA2) is highly expressed in a broad range of benign and malignant tumors.Virchows Archiv : an international journal of pathology · 2025Article
- Fusion of the High-mobility Group AT-Hook 2 (In vivo (Athens, Greece)Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimThe translocation t(9;12) (p22;q14~15) has been reported in lipomas, pleomorphic adenomas, a myolipoma, two chondroid hamartomas, and two uterine leiomyomas. In lipomas and pleomorphic adenomas, the translocation fuses HMGA2 (12q14) with the NFIB gene from 9p22; in myolipoma, it fuses HMGA2 with C9orf92 from 9p22; and in chondroid hamartomas, fluorescence in situ hybridization (FISH) investigations showed the chromosomal aberration to cause intragenic rearrangement of HMGA2. The translocation's molecular consequence in a uterine leiomyoma is described here. MATERIALS AND
methodsA typical leiomyoma was investigated using banding cytogenetics, FISH, RNA sequencing, reverse transcription polymerase chain reaction and Sanger sequencing.
resultsA single translocation, t(9;12)(p22;q14) leading to an HMGA2::BNC2 chimera, was found in tumor cells. A sequence of the untranslated part of exon 5 of HMGA2 (nucleotide 1035 in the NCBI reference sequence NM_003483.4) had fused with a sequence from the untranslated part of exon 7 of BNC2 from 9p22 (nucleotide 9284 in reference sequence NM_017637.6).
conclusionAt the molecular level, the t(9;12)(p22;q14~15) found in several benign tumors appears to be heterogeneous fusing HMGA2 with either BNC2, C9orf92 or NFIB which all three map close to one another within a 3 Mbp region in 9p22. Because the fusion point in HMGA2 in the present tumor lays downstream from the first Let-7 miRNA consensus binding site, we conclude that deletion of the first Let-7 miRNA binding site is not important for the transcriptional upregulation of HMGA2 caused by the genomic rearrangement.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.