ArticleNucleic acids research2016
Frequent occurrence of large duplications at reciprocal genomic rearrangement breakpoints in multiple myeloma and other tumors.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A complex reciprocal translocation is linked to reduced gamete viability in a loose-bunch grapevine somatic variant.BMC plant biology · 2026Article
- Linked-read whole-genome sequencing resolves common and private structural variants in multiple myeloma.Blood advances · 2022Article
- Chromatin Accessibility Identifies Regulatory Elements Predictive of Gene Expression and Disease Outcome in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Promiscuous Structural Variants Drive Myeloma Initiation and Progression.Blood cancer discovery · 2020Article
- Microhomology-mediated end joining drives complex rearrangements and overexpression ofHaematologica · 2020Article
- Functions and Clinical Significance of Super-Enhancers in Bone-Related Diseases.Frontiers in cell and developmental biology · 2020Review
- Mate pair sequencing outperforms fluorescence in situ hybridization in the genomic characterization of multiple myeloma.Blood cancer journal · 2019Article
- Multiple myeloma immunoglobulin lambda translocations portend poor prognosis.Nature communications · 2019Article
- Cell of Origin and Genetic Alterations in the Pathogenesis of Multiple Myeloma.Frontiers in immunology · 2019Review
- MB4-2/MB4-3 transcripts ofOncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Using a combination of array comparative genomic hybridization, mate pair and cloned sequences, and FISH analyses, we have identified in multiple myeloma cell lines and tumors a novel and recurrent type of genomic rearrangement, i.e. interchromosomal rearrangements (translocations or insertions) and intrachromosomal inversions that contain long (1-4000 kb; median ∼100 kb) identical sequences adjacent to both reciprocal breakpoint junctions. These duplicated sequences were generated from sequences immediately adjacent to the breakpoint from at least one-but sometimes both-chromosomal donor site(s). Tandem duplications had a similar size distribution suggesting the possibility of a shared mechanism for generating duplicated sequences at breakpoints. Although about 25% of apparent secondary rearrangements contained these duplications, primary IGH translocations rarely, if ever, had large duplications at breakpoint junctions. Significantly, these duplications often contain super-enhancers and/or oncogenes (e.g. MYC) that are dysregulated by rearrangements during tumor progression. We also found that long identical sequences often were identified at both reciprocal breakpoint junctions in six of eight other tumor types. Finally, we have been unable to find reports of similar kinds of rearrangements in wild-type or mutant prokaryotes or lower eukaryotes such as yeast.
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Registered trials
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