ArticleProceedings of the National Academy of Sciences of the United States of America1996
Promiscuous translocations into immunoglobulin heavy chain switch regions in multiple myeloma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 378 citations in OpenAlex.
- Article
- Review
- Temporal genomic dynamics shape clinical trajectory in multiple myeloma.Nature genetics · 2025Article
- Article
- Single-cell analysis of neoplastic plasma cells identifies myeloma pathobiology mediators and potential targets.Cell reports. Medicine · 2025Article
- Comprehensive molecular profiling of multiple myeloma identifies refined copy number and expression subtypes.Nature genetics · 2024Observational
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- ETV4-Dependent Transcriptional Plasticity Maintains MYC Expression and Results in IMiD Resistance in Multiple Myeloma.Blood cancer discovery · 2024Article
- Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma.Blood cancer discovery · 2024Article
- CDK6 protein expression is associated with disease progression and treatment resistance in multiple myeloma.HemaSphere · 2024Article
- Preclinical models for prediction of immunotherapy outcomes and immune evasion mechanisms in genetically heterogeneous multiple myeloma.Nature medicine · 2023Article
- Combination venetoclax and selinexor effective in relapsed refractory multiple myeloma with translocation t(11;14).NPJ precision oncology · 2022Article
- Multiple myeloma with high-risk cytogenetics and its treatment approach.International journal of hematology · 2022Review
- Single-cell gene fusion detection by scFusion.Nature communications · 2022Article
- Super Enhancer-Mediated Upregulation ofCancer research · 2022Article
- Review
- 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
- Review
- Review
- Promiscuous Structural Variants Drive Myeloma Initiation and Progression.Blood cancer discovery · 2020Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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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
In multiple myeloma, karyotopic 14q32 translocations have been identified at a variable frequency (10-60% in different studies). In the majority of cases, the partner chromosome has not been identified (14q+), and in the remaining cases, a diverse array of chromosomal partners has been implicated, with 11q13 being the most common. We developed a comprehensive Southern blot assay to identify and distinguish different kinds of immunoglobulin heavy chain (IgH) switch recombination events. Illegitimate switch recombination fragments (defined as containing sequences from only one switch region) are potential markers of translocation events into IgH switch regions and were identified in 15 of 21 myeloma cell lines, including seven of eight karyotyped lines that have no detectable 14q32 translocation. From all nine lines or tumor samples analyzed further, cloned illegitimate switch recombination fragments were confirmed to be IgH switch translocation breakpoints. In three of these cases, the translocation breakpoint was shown to be present in the primary tumor. These translocation breakpoints involve six chromosomal loci: 4p16.3 (two lines and the one tumor); 6; 8q24.13; 11q13.3 (in three lines); 16q23.1; and 21q22.1. We suggest that translocations into the IgH locus (i) are frequent (karyotypic 14q32 translocations and/or illegitimate switch recombination fragments are present in primary tumor samples and in 19 of 21 lines that we have analyzed); (ii) occur mainly in switch regions; and (iii) involve a diverse but nonrandom array (i.e., frequently 11q13 or 4p16) of chromosomal partners. This appears to be the most frequent genetic abnormality in multiple myeloma.
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