Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3
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Dysregulation of oncogenes by translocation to the IgH locus (14q32) is a seminal event in the pathogenesis of B-cell tumours. In multiple myeloma (MM), translocations to the IgH locus have been reported at an incidence of 20-60%. For most translocations, the partner chromosome is unknown (14q+); for the others, a diverse array of chromosomal partners have been identified, with 11q13 (cyclin D1) the only chromosome that is frequently involved. Recently, we developed a Southern-blot assay that detects translocation breakpoint fragments in most MM tumours, including those with no translocation detected by conventional karyotyping. In a continuing analysis of translocation in 21 myeloma cell lines and primary tumours, we show that the novel, karyotypically silent translocation t(4;14)(p16.3;q32.3) is present in five lines and at least three of ten primary tumours. The chromosome-4 breakpoints are clustered in a 70-kb region centromeric to the fibroblast growth factor receptor 3 gene (FGFR3), the apparent dysregulated oncogene. Two lines and one primary tumour with this translocation selectively express an FGFR3 allele containing activating mutations identified previously in thanatophoric dwarfism. We propose that after the t(4;14) translocation, somatic mutation during tumour progression frequently generates in FGFR3 protein that is active in the absence of ligand.
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Multiple myeloma and MGUS/SMM have two key groups of initiating events: immunoglobulin (IGH) translocations and hyperdiploidy (HY).
“Historically, MM and MGUS/SMM have two key groups of initiating events: immunoglobulin (IGH) translocations and hyperdiploid (HY).9,54-59”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [56]
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“The translocations usually result in dysregulated expression of several heterogeneous partners including c-myc, cyclin D1 (Chesi et al., 1996), c-maf (Chesi et al., 1998a), and FGFR3 (Chesi et al., 1997).”
BackgroundSelf-citation
- Authors
- Chesi, M., Nardini, E., Brents, L. A., Schröck, E., Ried, T., Kuehl, W. M., & Bergsagel, P. L.
- Affiliations
- National Institutes of Health (US)
- Cornell University (US)
- Corresponding author
- Kuehl, W. Michael
- Venue
- Nature Genetics
- Published
- 1997-07
- Volume
- 16
- Issue
- 3
- Pages
- 260-264
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3901950
- OpenAlex
- W2054290966
- Cited by
- 637
- References
- 0
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 13 · 2023: 14 · 2022: 11 · 2021: 11 · 2020: 14 · 2019: 16 · 2018: 13 · 2017: 13 · 2016: 19 · 2015: 15 · 2014: 23 · 2013: 21 · 2012: 26
- FWCI
- 17.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (K01CA074265)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Health Sciences › Medicine › Rheumatology › Bone Tumor Diagnosis and Treatments
- Keywords
- multiple myeloma, FGFR3, activating mutations, somatic mutations, myeloma cell lines, thanatophoric dwarfism
- MeSH terms
- Chromosomes, Human, Pair 14, Chromosomes, Human, Pair 4, Humans, Karyotyping, Molecular Sequence Data, Multiple Myeloma, Mutation, Oncogenes, Protein-Tyrosine Kinases, RNA, Messenger, Translocation, Genetic, Tumor Cells, Cultured, Blotting, Southern, Immunoblotting, Blotting, Northern, DNA Probes, Gene Expression Regulation, Neoplastic, Polymerase Chain Reaction, In Situ Hybridization, Fluorescence, Receptors, Fibroblast Growth Factor, Receptor, Fibroblast Growth Factor, Type 3
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