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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Krejčí, P. (2013) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2013.11.001 · Cited by 51
Staging and prognostication of multiple myeloma
Fonseca, R., Monge, J., & Dimopoulos, M. A. (2014) · Expert Review of Hematology · doi:10.1586/17474086.2014.882224 · Cited by 39
“The t(4;14)(p16;q32) is associated with FGFR3 and MMSET dysregulation [50], while t(14;16) (q32;q23) is associated with increased c-maf expression [51].”
Ligand activation leads to regulated intramembrane proteolysis of fibroblast growth factor receptor 3
Degnin, C., Laederich, M. B., & Horton, W. (2011) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-01-0080 · Cited by 48
“In contrast, similar somatic mutations have been detected in several neoplasias, including multiple myeloma (Chesi et al., 1997; Richelda et al., 1997), bladder cancer (Chaffer et al.”
Background
Genomics in multiple myeloma
Munshi, N., & Avet-Loiseau, H. (2011) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-10-1843 · Cited by 48
A Review of Angiogenesis and Anti-Angiogenic Therapy in Hematologic Malignancies
Rajkumar, S. V., Mesa, R. A., & Tefferi, A. (2002) · Stem Cells and Development · doi:10.1089/152581602753448522 · Cited by 40
Expression of fibroblast growth factor receptor family members is associated with prognosis in early stage cervical cancer patients
Choi, C., Chung, J., Kim, J.-H., Kim, B.-G., & Hewitt, S. (2016) · Journal of Translational Medicine · doi:10.1186/s12967-016-0874-0 · Cited by 47
“Furthermore, activating mutations and overexpression of FGFR3 have been reported in bladder cancers [17] and multiple myeloma [18].”
Background
A novel FGFR3-binding peptide inhibits FGFR3 signaling and reverses the lethal phenotype of mice mimicking human thanatophoric dysplasia.
Jin, M., Yu, Y., Qi, H.-B., Xie, Y.-L., Su, N., Wang, X.-F., Tan, Q.-Y., Luo, F.-T., Zhu, Y., Wang, Q., et al. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds390 · Cited by 47
Detection of N-Ras codon 61 mutations in subpopulations of tumor cells in multiple myeloma at presentation
Kalakonda, N., Rothwell, D. G., Scarffe, J. H., & Norton, J. D. (2001) · Blood · doi:10.1182/blood.v98.5.1555 · Cited by 41
Fibroblast Growth Factor Receptor 3 Induces Gene Expression Primarily through Ras-independent Signal Transduction Pathways*
Choi, D., Toledo-Aral, J., Lin, H.-Y., Ischenko, I., Medina, L., Safo, P. K., Mandel, G., Levinson, S. R., Halegoua, S., & Hayman, M. J. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m002959200 · Cited by 46
The inositol phosphatase SHIP2 enables sustained ERK activation downstream of FGF receptors by recruiting Src kinases
Fafílek, B., Bálek, L., Bosakova, M. K., Vařecha, M., Niţă, A., Gregor, T., Gudernová, I., Křenová, J., Ghosh, S., Piskáček, M., et al. (2018) · Science Signaling · doi:10.1126/scisignal.aap8608 · Cited by 61
Elucidation of a four-site allosteric network in fibroblast growth factor receptor tyrosine kinases
Chen, H.-B., Marsiglia, W., Cho, M.-K., Huang, Z.-F., Deng, J.-J., Blais, S., Gai, W.-M., Bhattacharya, S., Neubert, T., Traaseth, N., et al. (2017) · eLife · doi:10.7554/elife.21137 · Cited by 44
“…mutations give rise to many forms of human congenital skeletal disorders of varying clinical severity and acquired cancers (Wilkin et al., 2001; Wilkie, 2005; Webster and Donoghue, 1997; PassosBueno et al., 1999; Rand et al., 2005; Chesi et al., 1997; Richelda et al., 1997; Cappellen et al., 1999).”
Background
FGFR3 has tumor suppressor properties in cells with epithelial phenotype
Lafitte, M., Moranvillier, I., Garcia, S., Peuchant, E., Iovanna, J., Rousseau, B., Dubus, P., Guyonnet-Duperat, V., Belléannée, G., Ramos, J., et al. (2013) · Molecular Cancer · doi:10.1186/1476-4598-12-83 · Cited by 44
FGFR3 targeting strategies for achondroplasia
Laederich, M. B., & Horton, W. (2012) · Expert Reviews in Molecular Medicine · doi:10.1017/erm.2012.4 · Cited by 44
“14 Chesi, M. et al. (1997) Frequent translocation t(4;14)(p16.”
Preclinical activity of a novel multiple tyrosine kinase and aurora kinase inhibitor, ENMD‐2076, against multiple myeloma
Wang, X., Sinn, A. L., Pollok, K. E., Sandusky, G. E., Zhang, S., Chen, L., Liang, J., Crean, C., Suvannasankha, A., Abonour, R., et al. (2010) · British Journal of Haematology · doi:10.1111/j.1365-2141.2010.08248.x · Cited by 48
“The t(4;14) results in ectopic expression of functional FGFR-3 on MM cells, which otherwise do not express it (Chesi et al, 1997, 2001).”
Background
Genomic aberrations in plasma cell leukemia shown by interphase fluorescence in situ hybridization.
Chang, H., Sloan, S., Li, D., & Patterson, B. (2005) · Cancer Genetics and Cytogenetics · doi:10.1016/j.cancergencyto.2004.05.004 · Cited by 44
Light-chain only multiple myeloma is due to the absence of functional (productive) rearrangement of the IgH gene at the DNA level.
Magrangeas, F., Cormier, M., Descamps, G., Gouy, N., Lodé, L., Mellerin, M., Harousseau, J., Bataille, R., Minvielle, S., & Avet-Loiseau, H. (2004) · Blood · doi:10.1182/blood-2003-07-2501 · Cited by 44
“Of note, whereas the colocalization of the FGFR3 and IgH probes was observed in all 5 cases with t(4;14), colocalization of the CCND1 and IgH probes was seen in only 5 of the 9 cases with t(11;14), probably because of the scattering of the 11q13 breakpoints over a much larger distance.”
Influential
No evidence of somatic FGFR3 mutation in various types of carcinoma
Karoui, M., Hofmann-Radvanyi, H., Zimmermann, U., Couvelard, A., Degott, C., Faridoni-Laurens, L., Ahomadegbe, J., Gazzeri, S., Brambilla, E., Clérici, T., et al. (2001) · Oncogene · doi:10.1038/sj.onc.1204651 · Cited by 44
“…those found in thanatophoric dysplasia (neonatal lethal dwar®sm syndrome) and a related genetic disease SADDAN were shown to be associated with rare cases of multiple myeloma (Chesi et al., 1997; Richelda et al., 1997) and more recently with bladder and cervical carcinomas (Cappellen et al., 1999).”
Background
Three-Dimensional Genome Architecture Influences Partner Selection for Chromosomal Translocations in Human Disease
Engreitz, J., Agarwala, V., & Mirny, L. A. (2012) · PLoS ONE · doi:10.1371/journal.pone.0044196 · Cited by 132
FGFR3 and PIK3CA mutations in stucco keratosis and dermatosis papulosa nigra
Hafner, C., Landthaler, M., Mentzel, T., & Vogt, T. (2010) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2009.09488.x · Cited by 43
Clinical implications of chromosomal abnormalities in multiple myeloma
Terpos, E., Eleutherakis-Papaiakovou, V., & Dimopoulos, M. A. (2006) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.1080/10428190500464104 · Cited by 52
“3;q32) is karyotypically cryptic and was first described in human MM cell lines [46].”
Background
Constitutively activated FGFR3 mutants signal through PLCgamma-dependent and -independent pathways for hematopoietic transformation.
Chen, J., Williams, I., Lee, B. H., Duclos, N., Huntly, B. J. P., Donoghue, D. J., & Gilliland, D. G. (2004) · Blood · doi:10.1182/blood-2004-09-3686 · Cited by 41
A molecular study of the t(4;14) in multiple myeloma
Sibley, K., Fenton, J., Dring, A., Ashcroft, A. J., Rawstron, A., & Morgan, G. (2002) · British Journal of Haematology · doi:10.1046/j.1365-2141.2002.03618.x · Cited by 41
“FGFR3 mutations that constitutively activate the receptor in a ligand independent manner have been frequently found in both bladder and cervical cancers (Cappellen et al, 1999; Sibley et al, 2001), and also in myeloma cell lines (Chesi et al, 1997, 1998; Richelda et al, 1997).”
Background
Fluorescence in situ hybridization analysis shows the frequent occurrence of 14q32.3 rearrangements with involvement of immunoglobulin switch regions in myeloma cell lines.
Kuipers, J., Vaandrager, J., Weghuis, D., Pearson, P. L., Scheres, J., Lokhorst, H., Clevers, H. C., & Bast, B. J. E. G. (1999) · Cancer Genetics and Cytogenetics · doi:10.1016/s0165-4608(98)00157-5 · Cited by 41
Infrequent frameshift mutations of polynucleotide repeats in multiple primary cancers affecting the esophagus and other organs
Iwaya, T., Maesawa, C., Nishizuka, S., Suzuki, Y., Sakata, K., Sato, N., Ikeda, K., Koeda, K., Ogasawara, S., Otsuka, K., et al. (1998) · Genes Chromosomes and Cancer · doi:10.1002/(sici)1098-2264(199812)23:4 · Cited by 12
Genetic alterations of FGF receptors: an emerging field in clinical cancer diagnostics and therapeutics
Katoh, M. (2010) · Expert Review of Anticancer Therapy · doi:10.1586/era.10.128 · Cited by 44
FGFR3-targeted mAb therapy for bladder cancer and multiple myeloma.
Hadari, Y., & Schlessinger, J. (2009) · Journal of Clinical Investigation · doi:10.1172/jci38948 · Cited by 40
FGFR3 gene mutations associated with human skeletal disorders occur rarely in multiple myeloma.
Fracchiolla, N., Luminari, S., Baldini, L., Lombardi, L., Maiolo, A., & Neri, A. (1998) · Blood · doi:10.1182/blood.v92.8.2987 · Cited by 40
Therapeutic uses of FGFs
Zhang, J., & Li, Y. (2015) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2015.09.007 · Cited by 44
FGFR3 Mutations and the Skin: Report of a Patient with a FGFR3 Gene Mutation, Acanthosis Nigricans, Hypochondroplasia and Hyperinsulinemia and Review of the Literature
Blomberg, M., Jeppesen, E. M., Skovby, F., & Benfeldt, E. (2010) · Dermatology · doi:10.1159/000297575 · Cited by 39
Pleiotropic anti-myeloma activity of ITF2357: inhibition of interleukin-6 receptor signaling and repression of miR-19a and miR-19b
Todoerti, K., Barbui, V., Pedrini, O., Lionetti, M., Fossati, G., Mascagni, P., Rambaldi, A., Neri, A., Introna, M., Lombardi, L. T., et al. (2009) · Haematologica · doi:10.3324/haematol.2009.012088 · Cited by 38
Nordihydroguaiaretic Acid Inhibits an Activated FGFR3 Mutant, and Blocks Downstream Signaling in Multiple Myeloma Cells
Meyer, A. N., McAndrew, C. W., & Donoghue, D. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-0575 · Cited by 39
FGFR3 Mutations in Benign Skin Tumors
Hafner, C., Vogt, T., & Hartmann, A. (2006) · Cell Cycle · doi:10.4161/cc.5.23.3509 · Cited by 39
The enigma of ectopic expression of FGFR3 in multiple myeloma: a critical initiating event or just a target for mutational activation during tumor progression
Chesi, M., Bergsagel, P. L., & Kuehl, W. M. (2002) · Current Opinion in Hematology · doi:10.1097/00062752-200207000-00005 · Cited by 36
Self-citation
Fibroblast growth factor receptor 3 activates a network of profibrotic signaling pathways to promote fibrosis in systemic sclerosis
Chakraborty, D., Zhu, H., Jüngel, A., Summa, L., Li, Y., Matei, A., Zhou, X., Huang, J., Trinh‐Minh, T., Chen, C.-W., et al. (2020) · Science Translational Medicine · doi:10.1126/scitranslmed.aaz5506 · Cited by 53
Genome-wide haplotype association study identify the FGFR2 gene as a risk gene for Acute Myeloid Leukemia
Lv, H., Zhang, M., Shang, Z., Li, J., Zhang, S., Lian, D., & Zhang, R. (2016) · Oncotarget · doi:10.18632/oncotarget.13631 · Cited by 38
NF449 Is a Novel Inhibitor of Fibroblast Growth Factor Receptor 3 (FGFR3) Signaling Active in Chondrocytes and Multiple Myeloma Cells*
Krejci, P., Murakami, S., Procházková, J., Trantírek, L., Chlebová, K., Ouyang, Z.-F., Aklian, A., Smutny, J., Bryja, V., Kozubík, A., et al. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.083626 · Cited by 38
Transcriptional Heterogeneity Overcomes Super-Enhancer Disrupting Drug Combinations in Multiple Myeloma
Welsh, S. J., Barwick, B. G., Meermeier, E. W., Riggs, D. L., Shi, C.-X., Zhu, Y. X., Sharik, M. E., Du, M. T., Rocha, L. D. A., Garbitt, V. M., et al. (2023) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-23-0062 · Cited by 44
Self-citation
Molecular and immunological mechanisms of clonal evolution in multiple myeloma
Forster, S., Radpour, R., & Ochsenbein, A. F. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1243997 · Cited by 44
“3;q32) results in the overexpression of the fibroblast-growth factor receptor 3 (FGFR3) and can be detected in about 15% of all myeloma patients (61, 123).”
Background
Discovery and optimization of novel pyrazole-benzimidazole CPL304110, as a potent and selective inhibitor of fibroblast growth factor receptors FGFR (1–3)
Yamani, A., Zdżalik-Bielecka, D., Lipner, J., Stanczak, A. M., Piórkowska, N., Stańczak, P. S., Olejkowska, P., Hucz‐Kalitowska, J., Magdycz, M., Dzwonek, K., et al. (2020) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2020.112990 · Cited by 49
Phase 2 study of dovitinib in patients with relapsed or refractory multiple myeloma with or without t(4;14) translocation
Scheid, C., Reece, D. E., Beksaç, M., Spencer, A. G., Callander, N. S., Sonneveld, P., Kalimi, G. H., Cai, C., Shi, M. M., Scott, J. W., et al. (2014) · European Journal Of Haematology · doi:10.1111/ejh.12491 · Cited by 36
Molecular pathogenesis of multiple myeloma
Furukawa, Y., & Kikuchi, J. (2015) · International Journal of Clinical Oncology · doi:10.1007/s10147-015-0837-0 · Cited by 67
Activating FGFR3 mutations cause mild hyperplasia in human skin, but are insufficient to drive benign or malignant skin tumors
Duperret, E. K., Oh, S., McNeal, A. S., Prouty, S., & Ridky, T. W. (2014) · Cell Cycle · doi:10.4161/cc.28492 · Cited by 37
Towards a new age in the treatment of multiple myeloma
Piazza, F., Gurrieri, C., Trentin, L., & Semenzato, G. (2007) · Annals of Hematology · doi:10.1007/s00277-006-0239-5 · Cited by 32
Translocation T(4;14)(p16.3;q32) is a recurrent genetic lesion in primary amyloidosis.
Perfetti, V., Coluccia, A., Intini, D., Malgeri, U., Vignarelli, M. C., Casarini, S., Merlini, G., & Neri, A. (2001) · American Journal of Pathology · doi:10.1016/s0002-9440(10)64115-6 · Cited by 37
Somatic mutations of fibroblast growth factor receptor 3 (FGFR3) are uncommon in carcinomas of the uterine cervix
Wu, R., Connolly, D., Ngelangel, C., Bosch, F., Muñoz, N., & Cho, K. R. (2000) · Oncogene · doi:10.1038/sj.onc.1203934 · Cited by 37
“In 1997, two independent groups provided data supporting a role for FGFR3 activation in human cancer (Chesi et al., 1997; Richelda et al., 1997).”
Background

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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