{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:56:30Z","timestamp":1791140190567,"version":"4.1.0"},"reference-count":49,"publisher":"American Society of Hematology","issue":"3","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The t(4;14) translocation occurs frequently in multiple myeloma (MM) and results in the simultaneous dysregulated expression of 2 potential oncogenes, FGFR3 (fibroblast growth factor receptor 3) from der(14) and multiple myeloma SET domain protein\/Wolf-Hirschhorn syndrome candidate gene 1 from der(4). It is now shown that myeloma cells carrying a t(4;14) translocation express a functional FGFR3 that in some cases is constitutively activated by the same mutations that cause thanatophoric dysplasia. As with activating mutations of K-ras and N-ras, which are reported in approximately 40% of patients with MM, activating mutations ofFGFR3 occur during tumor progression. However, the constitutive activation of ras and FGFR3 does not occur in the same myeloma cells. Thus the activated forms of these proteins appear to share an overlapping role in tumor progression, suggesting that they also share the signaling cascade. Consistent with this prediction, it is shown that activated FGFR3\u2014when expressed at levels similar to those seen in t(4;14) myeloma\u2014is an oncogene that acts through the MAP kinase pathway to transform NIH 3T3 cells, which can then generate tumors in nude mice. Thus,FGFR3, when overexpressed in MM, may be not only oncogenic when stimulated by FGF ligands in the bone marrow microenvironment, but is also a target for activating mutations that enable FGFR3to play a ras-like role in tumor progression.<\/jats:p>","DOI":"10.1182\/blood.v97.3.729","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:47Z","timestamp":1027774007000},"page":"729-736","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":240,"title":["Activated fibroblast growth factor receptor 3 is an oncogene that contributes to tumor progression in multiple myeloma"],"prefix":"10.1182","volume":"97","author":[{"given":"Marta","family":"Chesi","sequence":"first","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leslie A.","family":"Brents","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah A.","family":"Ely","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Bais","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Davide F.","family":"Robbiani","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enrique A.","family":"Mesri","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. Michael","family":"Kuehl","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. Leif","family":"Bergsagel","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Division of Hematology-Oncology, New York Presbyterian Hospital\u2013Weill Medical College of Cornell University; the Immunology Program, Weill Graduate School of Medical Sciences of Cornell University, New York, NY; and the Genetics Department, Medicine Branch, National Cancer Institute, Bethesda, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2020021220081215500_B1","doi-asserted-by":"crossref","first-page":"13931","DOI":"10.1073\/pnas.93.24.13931","article-title":"Promiscuous translocations into IgH switch regions in multiple myeloma.","volume":"93","author":"Bergsagel","year":"1996","journal-title":"Proc Natl Sci Acad U S A."},{"key":"2020021220081215500_B2","doi-asserted-by":"crossref","first-page":"4457","DOI":"10.1182\/blood.V91.12.4457","article-title":"Frequent dysregulation of the c-maf proto-oncogene at 16q23 by 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