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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Research works printed but not linked: 31

Korsmeyer, S.J. Chromosomal translations in lymphoid malignancies reveal novel proto-oncogenes. Annu. Rev. Immunol. 10, 785–607 (1992). · DOI
Taniwaki, M. et al. Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia. Blood 84, 2283–2290 (1994). · DOI
Sawyer, J.R., Waldron, J.A., Jagannath, S. & Barlogie, B. Cytogenetic findings in 200 patients with multiple myeloma. Cancer Genet. Cytogenet. 82, 41–49 (1995). · DOI
Lai, J.L. et al. Improved cytogenetics in multiple-myeloma—a study of 151 patients including 117 patients at diagnosis. Blood 85, 2490–2497 (1995). · DOI
Chesi, M. et al. Dysregulation of Cyclin D1 by translocation into an IgH gamma switch region in two multiple myeloma cell lines. Blood 88, 674–681 (1996). · DOI
Bergsagel, P.L. et al. Promiscuous translations into IgH switch regions in multiple myeloma. Proc. Natl. Sci. Acad. USA 93, 13931–13936 (1996). · DOI · Paper page
Baxendale, S. et al. A cosmid contig and high resolution restriction map of the 2 megabase region containing the Huntington's disease gene. Nature Genet. 4, 181–186 (1993). · DOI
Keegan, K., Johnson, D., William, L.T. & Hayman, M.J. Isolation of an additional member of the fibroblast growth factor receptor family, FGFR-3. Proc. Natl. Acad Sci. USA 88, 1095–1099(1991). · DOI
Keegan, K., Meyer, S. & Hayman, M.J. Structural and biosynthetic characterization of the fibroblast growth factor receptor 3 (FGFR-3) protein. Oncogene 6, 2229–2236 (1991).
Muenke, M. & Schell, U. Fibroblast-growth-factor-receptor mutations in human sketetal disorders. Trends Genet. 11, 308–313 (1995). · DOI
Naski, M.C., Wang, Q., Xu, J. & Ornitz, D.M. Graded activation of fibroblast growth factor receptor 3 by mutations causing achondroplasia and thanatophoric dysplasia. Nature Genet. 13, 233–237 (1996). · DOI
Webster, M.K., D'Avis, P.Y., Robertson, S.C. & Donoghue, D.J. Profound ligand-independent kinase activation of fibroblast growth factor receptor 3 by the activation loop mutation responsible for a lethal skeletal dysplasia, thanatophoric dysplasia type II. Mol. Cell. Biol. 16, 4081–4087 (1996). · DOI
Webster, M.K. & Donoghue, D.J. Constitutive activation of fibroblast growth factor receptor 3 by the transmembrane domain point mutation found in achondroplasia. EMBO J. 15, 520–527 (1996). · DOI
Rousseau, F. et al. Missense FGFR3 mutations create cysteine residues in thanatophoric dwarfism typeI (TD1). Hum. Mol. Genet. 5, 509–512 (1996). · DOI
Francomano, C.A. et al. A new skeletal dysplasia with severe tibial bowing, profound developmental delay and acanthosis nigricans is caused by a Lys 650 Met mutation in fibroblast growth factor receptor 3 (FGFR3). Am. J. Hum. Genet. 59, A25 (1996).
Tavormina, P.L. et al. Thanatophoric dysplasia (types I and II) caused by distinct mutations in fibroblast growth factor receptor 3. Nature Genet. 9, 321–328 (1995). · DOI
Williams, M.E., Swerdlow, S.H. & Meeker, T.C. Chromosome t(11;14)(q13;q32) breakpoints in centrocytic lymphoma are highly localized at the bcl-1 major translocation cluster. Leukemia 7, 1437–1440 (1993).
Tsujimoto, Y. et al. Clustering of breakpoints on chromosome 11 in human B-cell neoplasms with the t(11;14) chromosome translocation. Nature 315, 340–343 (1985). · DOI
de Boer, C.J. et al. Multiple breakpoints within the BCL-1 locus in B-cell lymphoma: rearrangements of the cyclin D1 gene. Cancer Res. 53, 4148–4152 (1993).
Mason, I.J. The ins and outs of fibroblast growth factors. Cell 78, 547–552 (1994). · DOI
Su, W.S. et al. Activation of Stat1 by mutant fibroblast growth-factor receptor in thanatophoric dysplasia type II dwarfism. Nature 386, 288–292 (1997). · DOI
Colvin, J.S., Bohne, B.A., Harding, G.W., McEwen, D.G. & Ornitz, D.M. Skeletal overgrowth and deafness in mice lacking fibroblast growth factor receptor 3. Nature Genet. 12, 390–397 (1996). · DOI
Deng, C., Wynshaw-Boris, A., Zhou, F., Kuo, A. & Leder, P. Fibroblast growth factor receptor 3 is a negative regulator of bone growth. Cell 84, 911–921 (1996). · DOI
Ornitz, D.M. & Leder, P. Ligand specificity and heparin dependence of fibroblast growth factor receptors 1 and 3. J. Biol. Chem. 267, 16305–16311 (1992). · DOI
Caligaris-Cappio, F. et al. Role of bone marrow stromal cells in the growth of human multiple myeloma. Blood 77, 2688–2693 (1991). · DOI
Allouche, M. Basic fibroblast growth factor and hematopoiesis. Leukemia 9, 937–942 (1995).
Shiang, R. et al. Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia. Cell 78, 335–342 (1994). · DOI
Johnston, C.L., Cox, H.C., Gomm, J.J. & Coombes, R.C. Fibroblast growth factor receptors (FGFRs) localize in different cellular compartments. J. Biol. Chem. 270, 30643–30650 (1995). · DOI
Schröck, E. et al. Multicolor spectral karyotyping of human chromosomes. Science 273, 494–497 (1996). · DOI
Kuehl, W.M., Brents, L.A., Chesi, M. & Bergsagel, P.L. Selective expression of one c-myc allele in two human myeloma cell lines. Cancer Res. 56, 4370–4373 (1996).
Davis, L.G., Kuehl, W.M. & Battey, J.F., Methods in Molecular Biology (Appleton & Lange, Norwalk, Connecticut, 1994).

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Campbell, L. J. (2011) · Methods in molecular biology · doi:10.1007/978-1-61779-074-4_2 · Cited by 2
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Cook, J. (2010) · doi:10.1007/978-1-4419-5698-9_19 · Cited by 1
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Anderson, K., Alsina, M., Bensinger, W., Biermann, J., Chanan-Khan, A., Cohen, A., Devine, S., Djulbegovic, B., Faber, E., Gasparetto, C., et al. (2001) · Bone Marrow Transplantation · doi:10.1038/sj.bmt.1702896 · Cited by 1
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Kern, F. (1999) · doi:10.1007/978-1-59259-456-6_3 · Cited by 1
Aberrant type I and type III collagen gene expression in human breast cancerin vivo
Kauppila, S., Stenbäck, F., Risteli, J., Jukkola, A., & Risteli, L. (1998) · The Journal of Pathology · doi:10.1002/(sici)1096-9896(1998110)186:3
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Gruber, E., Kumar, S., Franich, R. L., Khong, T., Neville, D., Ang, C.-S., The, J., Rumler, B., Alex, S., Dobbs, G., et al. (2026) · bioRxiv · doi:10.64898/2026.06.17.733047
Self-citation
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Self-citation
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Rheinheimer, B., Heimark, R., Grant, A. D., Camacho, L., Padi, M., & Jie, T. (2020) · bioRxiv · doi:10.1101/2020.09.29.318873
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Fend, F. (2018) · Springer eBooks · doi:10.1007/978-3-540-85184-4_9
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Background
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Self-citation
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Silencing Immunoglobulin Gene Enhancers as a Potential Treatment Strategy for Multiple Myeloma
Toman, I., Loree, J., Duerksen, K., Evans, R. P., & Reiman, T. (2008) · doi:10.7939/r3v06w
[Comparison of the rate of detection of immunoglobulin heavy chain gene rearrangement by fluoresecence in situ hybridization probes in multiple myeloma.].
Chung, H. Y., Cha, J.-S., Choi, J.-E., Min, H., Han, I.-C., & Lee, D. S. (2006) · The Korean Journal of Laboratory Medicine · doi:10.3343/kjlm.2006.26.5.317
Establishment and characterization of a new human myeloma cell line, KYδ-1, producing the δ/κ type immunoglobulin
Ueda, C., Yamada, H., Akasaka, T., Ohmori, K., Sasada, M., Uchiyama, T., & Ohno, H. (2001) · doi:10.1016/s0165-4608(01)00467-8
From chondrocytes to cancer: Fibroblast growth factor receptor 3 (FGFR3)
Guise, T. (2001) · doi:10.1138/2001016
Kleinzellige B-Zell-Lymphome: Differentialdiagnostische Leitlinien
Coupland, S. E., Dallenbach, F., & Stein, H. (2000) · Der Pathologe · doi:10.1007/s002920050382
Molecular and cytogenetic basis of lymphoid malignacies
Taniwaki, M. (1999) · doi:10.3960/jslrt1997.39.219
MULTIPLE MYELOMA
Coley, W. (1931) · Nursing Standard · doi:10.7748/ns.28.39.18.s22
Genomic instability in Multiple Myeloma-relevance for Clinical Outcome and Efficacy of Therapy
Sun, F., Cheng, Y., & Janz, S. (2019) · Blood and Genomics · doi:10.46701/apjbg.2019022019126
“From the cytogenetic perspective, recently reviewed by Kumar and Rajkumar ([27]), MM can broadly be divided into neoplasms that harbor either a hyper-diploid genome due to trisomy that preferentially involves odd chromosomes, or a pseudo-or hypo-diploid genome that contains a balanced (reciprocal) chromosomal transloc…”
Background
Prognosis of Myeloma/Genetics of Myeloma
Robiou-du-Pont, S., Corre, J., & Avet‐Loiseau, H. (2017) · Springer eBooks · doi:10.1007/978-3-319-64263-5_35
Cytogenetics of Plasma Cell Neoplasms
Sawyer, J. R. (2016) · Springer eBooks · doi:10.1007/978-3-319-42370-8_4
MicroRNAs in Hematologic Malignancies
Bloehdorn, J., ROUHI, A. M., Dhanyamraju, P. K., Krowiorz, K., Schneider, E. M., Langer, C., Mertens, D., Stilgenbauer, S., & Kuchenbauer, F. C. (2013) · Springer eBooks · doi:10.1007/978-1-4614-8444-8_5
Molecular Diagnostics of Lymphoid Neoplasms
Peker, D., Tao, J., & Zhang, L. (2013) · Springer eBooks · doi:10.1007/978-94-007-7192-5_17 · Cited by 1
Prognostic Implication of Genetic Changes (Cytogenetics, and FISH, Gains and Losses of DNA by SNP Array and aCGH) in Risk Stratification in Myeloma
Corre, J., & Avet-Loiseau, H. (2013) · doi:10.1007/978-1-4614-4666-8_2
Genetic Approaches to Study Transcriptional Activation and Tumor Suppression: A Dissertation
Lin, L. (2012) · eScholarship@UMassChan · doi:10.13028/q44r-af46
Signalling Molecules as Selective Targets for Therapeutic Strategies in Multiple Myeloma
Piazza, F., & Semenzato, G. (2011) · Springer eBooks · doi:10.1007/978-1-4614-0730-0_5
Fibroblast growth factor-2, chemoresistance and colorectal cancer
Prabhudesai, S. (2012) · doi:10.25560/10163
“Evidence from other studies also suggests that FGFRs are involved in several and sometimes opposing functions requiring tight regulation of their expression (242-244).”
Result
CHAPTER 30 – Abnormalities in immunoglobulin synthesizing cells
Davies, F., & Anderson, K. (2011) · doi:10.1016/b978-0-7020-3147-2.00030-4
Plasma Cell Myeloma and Other Plasma Cell Dyscrasias
Yared, M. A. (2009) · Humana Press eBooks · doi:10.1007/978-1-60761-384-8_19 · Cited by 1
Signaling from Fibroblast Growth Factor Receptors in Development and Disease
Drafahl, K. A., McAndrew, C. W., & Donoghue, D. (2010) · doi:10.1016/b978-0-12-374145-5.00237-0
Fibroblast Growth Factor Receptor 3 and Multiple Myeloma
Jimenez-Zepeda, V., & Stewart, A. (2008) · doi:10.1007/978-1-59745-564-0_23
Basic Biology of Plasma Cell Dyscrasias: Focus on the Role of the Tumor Microenviroment
Raab, M. S., & Anderson, K. C. (2008) · Humana Press eBooks · doi:10.1007/978-1-59745-564-0_3
Cytogenetic Abnormalities in Multiple Myeloma: The Importance of FISH and Cytogenetics
Braggio, E., Sebag, M., & Fonseca, R. (2008) · doi:10.1007/978-1-59745-564-0_5
Cytokines in Multiple Myeloma
de Vos, J., & Klein, B. (2004) · doi:10.1007/978-1-59259-817-5_5
Niedrigmaligne B-Zell-Lymphome
Mullerhermelink, H., & Ott, G. (2003) · Springer eBooks · doi:10.1007/978-3-642-59343-7_14
ACTIVATION MECHANISM OF FIBROBLAST GROWTH FACTOR RECEPTOR TYROSINE KINASE REVEALED BY CRYSTAL STRUCTURE OF FIBROBLAST GROWTH FACTOR RECEPTOR ECTODOMAIN BOUND TO FIBROBLAST GROWTH FACTOR AND HEPARIN.
Pellegrini, L., Burke, D., & Blundell, T. (2002) · doi:10.1007/0-306-47582-0_15
Mechanisms of B Cell Neoplasia 1998
Melchers, F., & Potter, M. (1999) · Current Topics in Microbiology and Immunology · doi:10.1007/978-3-642-60162-0

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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