Skip to main content
Log in

Concurrent JAK2(V617F) mutation and BCR-ABL translocation within committed myeloid progenitors in myelofibrosis

  • Letter to the Editor
  • Published:
Leukemia Submit manuscript

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Figure 1

References

  1. Barosi G, Ambrosetti A, Finelli C, Grossi A, Leoni P, Liberato NL et al. The Italian Consensus Conference on Diagnostic Criteria for Myelofibrosis with Myeloid Metaplasia. Br J Haematol 1999; 104: 730–737.

    Article  CAS  Google Scholar 

  2. Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 2005; 365: 1054–1061.

    Article  CAS  Google Scholar 

  3. James C, Ugo V, Le Couedic JP, Staerk J, Delhommeau F, Lacout C et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 434: 1144–1148.

    Article  CAS  Google Scholar 

  4. Kralovics R, Passamonti F, Buser AS, Teo SS, Tiedt R, Passweg JR et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 2005; 352: 1779–1790.

    Article  CAS  Google Scholar 

  5. Passamonti F, Rumi E, Pietra D, Della Porta MG, Boveri E, Pascutto C et al. Relation between JAK2 (V617F) mutation status, granulocyte activation, and constitutive mobilization of CD34+ cells into peripheral blood in myeloproliferative disorders. Blood 2006; 107: 3676–3682.

    Article  CAS  Google Scholar 

  6. Bellanne-Chantelot C, Chaumarel I, Labopin M, Bellanger F, Barbu V, De Toma C et al. Genetic and clinical implications of the Val617Phe JAK2 mutation in 72 families with myeloproliferative disorders. Blood 2006; 108: 346–352.

    Article  CAS  Google Scholar 

  7. Scott LM, Campbell PJ, Baxter EJ, Todd T, Stephens P, Edkins S et al. The V617F JAK2 mutation is uncommon in cancers and in myeloid malignancies other than the classic myeloproliferative disorders. Blood 2005; 106: 2920–2921.

    Article  CAS  Google Scholar 

  8. Jones AV, Kreil S, Zoi K, Waghorn K, Curtis C, Zhang L et al. Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders. Blood 2005; 106: 2162–2168.

    Article  CAS  Google Scholar 

  9. Biernaux C, Loos M, Sels A, Huez G, Stryckmans P . Detection of major bcr-abl gene expression at a very low level in blood cells of some healthy individuals. Blood 1995; 86: 3118–3122.

    CAS  PubMed  Google Scholar 

  10. Blickstein D, Aviram A, Luboshitz J, Prokocimer M, Stark P, Bairey O et al. BCR-ABL transcripts in bone marrow aspirates of Philadelphia-negative essential thrombocytopenia patients: clinical presentation. Blood 1997; 90: 2768–2771.

    CAS  PubMed  Google Scholar 

  11. Jamieson CH, Ailles LE, Dylla SJ, Muijtjens M, Jones C, Zehnder JL et al. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N Engl J Med 2004; 351: 657–667.

    Article  CAS  Google Scholar 

  12. Xie S, Wang Y, Liu J, Sun T, Wilson MB, Smithgall TE et al. Involvement of Jak2 tyrosine phosphorylation in Bcr-Abl transformation. Oncogene 2001; 20: 6188–6195.

    Article  CAS  Google Scholar 

Download references

Acknowledgements

We thank Anja Maiwald, Verona Schwarze, Jeanette Mundt, Ulrike Fitze, Marika Karger, Manuela Neumann and Cornelia Große for excellent technical assistance. Michelle Meredyth-Stewart is acknowledged for proofreading of this paper. This work was supported in part by the Deutsche Krebshilfe grant 70-2755 (MB and CT) and the Deutsche Forschungsgemeinschaft SFB 655 (MB, GE and CT).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to M Bornhäuser.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Bornhäuser, M., Mohr, B., Oelschlaegel, U. et al. Concurrent JAK2(V617F) mutation and BCR-ABL translocation within committed myeloid progenitors in myelofibrosis. Leukemia 21, 1824–1826 (2007). https://doi.org/10.1038/sj.leu.2404730

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.leu.2404730

  • Springer Nature Limited

This article is cited by

Navigation