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The JAK2 V617F tyrosine kinase mutation in myelodysplastic syndromes (MDS) developing myelofibrosis indicates the myeloproliferative nature in a subset of MDS patients

Leukemia volume 19, pages 2359–2360 (2005)Cite this article

TO THE EDITOR

The JAK2 V617F tyrosine kinase mutation is responsible for the development of BCR/ABL-negative chronic myeloproliferative disorders, including myelofibrosis (MF).1, 2, 3, 4 Kralovics et al1 demonstrated that 74% of patients with polycythemia vera (PV), 32% of essential thrombocythemia (ET), and 35% of patients with primary MF harbored the JAK2 V617F mutation. Recently, Steensma et al5 demonstrated that 5% (five of 101 patients) of myelodysplastic syndromes (MDS) patients had the JAK2 V617F tyrosine kinase mutation and reported its infrequent occurrence in other myeloid disorders, including MDS. However, the exact significance of the JAK2 V617F mutation in MDS is obscure. Myelofibrosis is associated with various hematologic diseases as a terminal hematologic condition and is an important issue in managing patients. Less than 10% of myelodysplastic syndromes (MDS) develop MF during their courses and most of them have unfavorable prognoses.6 The exact biology of MF in MDS patients is still unknown, since some MDS patients show aspects of both MDS and myeloproliferative disorders,7 and therefore, it is possible that MF could be associated with MDS as one phenotype of myelproliferative disorders.

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Acknowledgements

Thanks are due to Professor J Patrick Barron for his review of this manuscript and Mr Kunio Hori and Tohru Makino, NovusGene, Tokyo, for their technical assistance. This work was supported in part by a Grant-in-Aid for ‘Intractable Hematopoietic Diseases’ from the Ministry of Health, Welfare, and Labor, Japan (to KO), the ‘High-Tech Research Center’ Project from the Ministry of Education, Culture, Sports, Science and Technology: MEXT) (to KO, JHO), and by the ‘University-Industry Joint Research Project’ from MEXT (to KO, JHO).

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  1. The First Department of Internal Medicine, Tokyo Medical University, Tokyo, Japan

    K Ohyashiki, Y Aota, D Akahane, A Gotoh, K Miyazawa & Y Kimura

  2. Intractable Immune System Research Center, Tokyo Medical University, Tokyo, Japan

    J H Ohyashiki

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  1. K Ohyashiki
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Correspondence to K Ohyashiki.

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Ohyashiki, K., Aota, Y., Akahane, D. et al. The JAK2 V617F tyrosine kinase mutation in myelodysplastic syndromes (MDS) developing myelofibrosis indicates the myeloproliferative nature in a subset of MDS patients. Leukemia 19, 2359–2360 (2005). https://doi.org/10.1038/sj.leu.2403989

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