Accès gratuit
Numéro
Med Sci (Paris)
Volume 17, Numéro 11, Novembre 2001
Page(s) 1189 - 1191
Section Nouvelles
DOI https://doi.org/10.1051/medsci/200117111189
Publié en ligne 15 novembre 2001
  1. Schlessinger J. Cell signaling by receptor tyrosine kinases. Cell 2000; 103 : 211–25.
  2. Bonaventure J, Rousseau F, Legeai-Mallet L, et al. Récepteurs des facteurs de croissance fibroblastique (FGFR) et anomalies héréditaires de l’ossification enchondrale et membranaire. Med Sci 1996; 12 : 44–9.
  3. Webster MK, Donoghue DJ. FGFR activation in skeletal disorders: too much of a good thing. Trends Genet 1997; 13 : 178–82.
  4. Chesi M, Nardini E, Brents LA, et al. 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. Nat Genet 1997; 16 : 260–4
  5. Richelda R, Ronchetti D, Baldini L, et al. A novel chromosomal translocation t(4 ; 14)(p16.3 ; q32) in multiple myeloma involves the fibroblast growth-factor receptor 3 gene. Blood 1997; 90 : 4062–70.
  6. Fracchiolla NS, Luminari S, Baldini L, Lombardi L, Maiolo AT, Neri A. FGFR3 gene mutations associated with human skeletal disorders occur rarely in multiple myeloma. Blood 1998; 92 : 2987–9.
  7. Chesi M, Nardini E, Lim RS, Smith KD, Kuehl WM, Bergsagel PL. The t(4 ;14) translocation in myeloma dysregulates both FGFR3 and a novel gene, MMSET, resulting in IgH/MMSET hybrid transcripts. Blood 1998; 92 : 3025–34.
  8. Stec I, Wright TJ, van Ommen GJ, et al. WHSC1, a 90 kb SET domain-containing gene, expressed in early development and homologous to a Drosophila dysmorphy gene maps in the Wolf-Hirschhorn syndrome critical region and is fused to IgH in t(4 ;14) multiple myeloma. Hum Mol Genet 1998; 7 : 1071–82.
  9. Cappellen D, De Oliveira C, Ricol D, et al. Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas. Nat Genet 1999; 23 : 18–20.
  10. Billerey C, Chopin D, Aubriot-Lorton MH, et al. Frequent FGFR3 mutations in papillary non-invasive bladder (pTa) tumors. Am J Pathol 2001; 158 : 1955–9.
  11. Karoui M, Hofmann-Radvanyi H, Zimmermann U, et al. No evidence of somatic FGFR3 mutation in various types of carcinoma. Oncogene 2001; 20 : 5059–61.
  12. Lee R, Droller MJ. The natural history of bladder cancer. Implications for therapy. Urol Clin North Am 2000; 27 : 1–13, vii.
  13. Spruck CH, Ohneseit PF, Gonzalez-Zulueta M, et al. Two molecular pathways to transitional cell carcinoma of the bladder. Cancer Res 1994; 54 : 784–8.
  14. van Rhijn BW, Lurkin I, Radvanyi F, Kirkels WJ, van der Kwast TH, Zwarthoff EC. The fibroblast growth factor receptor 3 (FGFR3) mutation is a strong indicator of superficial bladder cancer with low recurrence rate. Cancer Res 2001; 61 : 1265–8.
  15. Sybley K, Cuthbert-Heavens D, Knowles MA. Loss of heterozygosity at 4p16.3 and mutation of FGFR3 in transitional cell carcinoma. Oncogene 2001; 20 : 686–91.
  16. Ronchetti D, Greco A, Compasso S, et al. Deregulated FGFR3 mutants in multiple myeloma cell lines with t(4 ;14) : comparative analysis of Y373C, K650E and the novel G384D mutations. Oncogene 2001; 20 : 3553–62.

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.