The first two authors contributed equally to this work.
Constitutive activating mutation of the FGFR3b in oral squamous cell carcinomas
Article first published online: 4 MAY 2005
Copyright © 2005 Wiley-Liss, Inc.
International Journal of Cancer
Volume 117, Issue 1, pages 166–168, 20 October 2005
How to Cite
Zhang, Y., Hiraishi, Y., Wang, H., Sumi, K.-s., Hayashido, Y., Toratani, S., Kan, M., Sato, J. D. and Okamoto, T. (2005), Constitutive activating mutation of the FGFR3b in oral squamous cell carcinomas. Int. J. Cancer, 117: 166–168. doi: 10.1002/ijc.21145
- Issue published online: 2 AUG 2005
- Article first published online: 4 MAY 2005
- Manuscript Accepted: 28 FEB 2005
- Manuscript Received: 8 NOV 2004
- Ministry of Education, Science, Sports, and Culture of Japan
- Smoking Research Foundation
- National Institutes of Health. Grant Number: P20 RR16463
- oral squamous cell carcinomas;
A G to T mutation at nucleotide position 2128 in the human FGFR3b coding region resulting in a Cys for Gly substitution (G697C) in the tyrosine kinase domain was observed in 62% (44/71) of oral squamous cell carcinomas (OSCC) examined. Immunostained FGFR3b was found in the cytoplasm of prickle cells in normal epithelia, and FGFR3b was localized in the cytoplasm and nucleus in non-FGFR3b mutant OSCC. Overexpressed FGFR3b protein on plasma membranes was noted in OSCC bearing the FGFR3b mutation. Enhanced tyrosine kinase activity of G697CFGFR3b was confirmed. Our results indicate that G697C is an activating mutation causing constitutive ligand-independent FGFR3b signaling. This mutation may be involved in the progression of OSCC and thus the FGFR3b coding sequence may have diagnostic or prognostic value for OSCC. © 2005 Wiley-Liss, Inc.