Cited by 637Multiple Myeloma Research and TreatmentsLymphoma Diagnosis and TreatmentBone Tumor Diagnosis and Treatments

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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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Chesi, Marta, Nardini, Elena, Brents, Leslie A., Schröck, Evelin, Ried, Thomas, Kuehl, W. Michael, Bergsagel, P. Leif·1997·Nature Genetics

DOI 10.1038/ng0797-260PMC PMC3901950

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Abstract

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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Background
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BackgroundInfluential
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Background
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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
ORCID: Chesi, Marta
Schröck, Evelin
Ried, Thomas
Bergsagel, P. Leif
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 1997-07
Volume: 16
Issue: 3
Pages: 260-264
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/ng0797-260
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 › Orthopedics and Sports Medicine › 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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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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