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 Prepublished online as a Blood First Edition Paper on September 11, 2003; DOI 10.1182/blood-2003-05-1690.

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Submitted May 30, 2003
Accepted August 5, 2003

FOP-FGFR1 tyrosine kinase, the product of a t(6;8) translocation, induces a fatal myeloproliferative disease in mice

Geraldine Guasch, Benedicte Delaval, Christine Arnoulet, Min-Jue Xie, Luc Xerri, Danielle Sainty, Daniel Birnbaum, and Marie-Josephe Pebusque*

Department of Molecular Oncology, INSERM, Unite 119, Marseille, France
Department of Hematology, Institut Paoli Calmettes, Marseille, France
Department of BioPathology, Institut Paoli Calmettes, Marseille, France
Department of Functional Genomics, INSERM-EMI0116, Marseille, France

* Corresponding author; email: pebusque{at}marseille.inserm.fr.

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 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 PLC{gamma}binding site.


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