|
|
Blood, 1 January 2004, Vol. 103, No. 1, pp. 309-312.
Prepublished online as a Blood First Edition Paper on September 11, 2003; DOI 10.1182/blood-2003-05-1690.
 Previous Article | Table of Contents | Next Article 
NEOPLASIA
Brief report
FOP-FGFR1 tyrosine kinase, the product of a t(6;8) translocation, induces a fatal myeloproliferative disease in mice
Géraldine Guasch,
Bénédicte Delaval,
Christine Arnoulet,
Min-Jue Xie,
Luc Xerri,
Danielle Sainty,
Daniel Birnbaum, and
Marie-Josèphe Pébusque
From the Institut National de la Santé et de la Recherche Médicale (INSERM) U 119, IFR 57, Marseille, France; Université de la Méditerranée, Marseille, France; Department of Hematology Institut Paoli Calmettes, Marseille, France; Department of BioPathology, Institut Paoli Calmettes, Marseille, France; and INSERM EMI-0116, IFR 57, Marseille, France.
Constitutive activation of aberrant fibroblast growth factor receptor 1 (FGFR1) kinase as a consequence of gene fusion such as FOP-FGFR1 associated with t(6; 8)(q27;p11-12) translocation, is the hallmark of an atypical aggressive stem cell myeloproliferative disorder (MPD) in humans. In this study, we show that expression of FOP-FGFR1 in primary bone marrow cells induced by retroviral transduction generates a MPD in mice. Constitutive FOP-FGFR1 kinase activity was both essential and sufficient to cause a chronic myeloproliferative syndrome in the murine bone marrow transplantation model. In contrast to the human disorder, lymphoproliferation and progression to acute phase were not observed. Lymphoid symptoms, however, appeared when onset of the disease was delayed as the result of mutation of FOP-FGFR1 at tyrosine 511, the phospholipase C  (PLC) binding site.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
A. Chase, F. H. Grand, and N. C. P. Cross
Activity of TKI258 against primary cells and cell lines with FGFR1 fusion genes associated with the 8p11 myeloproliferative syndrome
Blood,
November 15, 2007;
110(10):
3729 - 3734.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Dong, S. Kang, T.-L. Gu, S. Kardar, H. Fu, S. Lonial, H. J. Khoury, F. Khuri, and J. Chen
14-3-3 integrates prosurvival signals mediated by the AKT and MAPK pathways in ZNF198-FGFR1-transformed hematopoietic cells
Blood,
July 1, 2007;
110(1):
360 - 369.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T.-L. Gu, V. L. Goss, C. Reeves, L. Popova, J. Nardone, J. MacNeill, D. K. Walters, Y. Wang, J. Rush, M. J. Comb, et al.
Phosphotyrosine profiling identifies the KG-1 cell line as a model for the study of FGFR1 fusions in acute myeloid leukemia
Blood,
December 15, 2006;
108(13):
4202 - 4204.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. A. Weinreich, I. Lintmaer, L. Wang, H. D. Liggitt, M. A. Harkey, and C. A. Blau
Growth factor receptors as regulators of hematopoiesis
Blood,
December 1, 2006;
108(12):
3713 - 3721.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Delaval, S. Letard, H. Lelievre, V. Chevrier, L. Daviet, P. Dubreuil, and D. Birnbaum
Oncogenic Tyrosine Kinase of Malignant Hemopathy Targets the Centrosome
Cancer Res.,
August 15, 2005;
65(16):
7231 - 7240.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. Vainchenker and S. N. Constantinescu
A Unique Activating Mutation in JAK2 (V617F) Is at the Origin of Polycythemia Vera and Allows a New Classification of Myeloproliferative Diseases
Hematology,
January 1, 2005;
2005(1):
195 - 200.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Chen, D. J. DeAngelo, J. L. Kutok, I. R. Williams, B. H. Lee, M. Wadleigh, N. Duclos, S. Cohen, J. Adelsperger, R. Okabe, et al.
PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder
PNAS,
October 5, 2004;
101(40):
14479 - 14484.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
