ArticleMolecular cytogenetics2015
Terminal 18q deletions are stabilized by neotelomeres.
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 7 papers.
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Who cites it
7 citing papers in PubMed.
- Replication-Based Mechanism Underlies a Complex dup(18p)/del(18q) Rearrangement Not Derived From Parental Inversion.Molecular syndromology · 2026Article
- ATR blocks telomerase from converting DNA breaks into telomeres.Science (New York, N.Y.) · 2024Article
- A comprehensive map of hotspots of de novo telomere addition in Saccharomyces cerevisiae.Genetics · 2023Article
- A comprehensive map of hotspots of de novo telomere addition inbioRxiv : the preprint server for biology · 2023Article
- Mechanisms of structural chromosomal rearrangement formation.Molecular cytogenetics · 2022Review
- Alternative lengthening of telomeres in childhood neuroblastoma from genome to proteome.Nature communications · 2021Article
- Breakpoint mapping at nucleotide resolution in X-autosome balanced translocations associated with clinical phenotypes.European journal of human genetics : EJHG · 2019Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundAll human chromosomes are capped by tandem repeat (TTAGGG)n sequences that protect them against end-to-end fusion and are essential to chromosomal replication and integrity. Therefore, after a chromosomal breakage, the deleted chromosomes must be stabilized by retaining the telomere or acquiring a new cap, by telomere healing or telomere capture. There are few reports with molecular approaches on the mechanisms involved in stabilization of 18q terminal deletions.
resultsIn this study we analyzed nine patients with 18q terminal deletion identified by G-banding and genomic array. FISH using PNA probe revealed telomeric signals in all deleted chromosomes tested. We fine-mapped breakpoints with customized arrays and sequenced six terminal deletion junctions. In all six deleted chromosomes sequenced, telomeric sequences were found directly attached to the breakpoints. Little or no microhomology was found at the breakpoints and none of the breaks sequenced were located in low copy repeat (LCR) regions, though repetitive elements were found around the breakpoints in five patients. One patient presented a more complex rearrangement with two deleted segments and an addition of 17 base pairs (bp).
conclusionsWe found that all six deleted chromosomes sequenced were probably stabilized by the healing mechanism leading to a neotelomere formation.
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