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Polycythemia associated with the JAK2V617F mutation emerged during treatment of chronic myelogenous leukemia

Leukemia volume 21, pages 1103–1104 (2007)Cite this article

A gain-of-function mutation at codon 617(V617F) of the Janus kinase 2 (JAK2) gene has been reported in chronic myeloproliferative diseases. The JAK2V617F results in a valine to phenylalanine substitution causing constitutive activation of the JAK–STAT pathway. This in turn leads to proliferation of the hematopoietic cells.1 Jelinek et al.2 recently published results of a study of the first large series of Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) patients with the JAK2V617F mutation. The mutation was not found in 99 CML patients, including 55 imatinib-resistant patients.

Recently, we encountered a JAK2V617F- and Ph-positive CML patient being treated with imatinib that evolved to erythrocytosis needing phlebotomy during cytogenetic complete remission (CCR).

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References

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Authors and Affiliations

  1. Division of Hematology, Department of Internal Medicine, Nippon Medical School, Bunkyo-Ku, Tokyo, Japan. E-mail: inami@nms.ac.jp,

    M Inami, K Inokuchi, M Okabe, F Kosaka, Y Mitamura, H Yamaguchi & K Dan

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  1. M Inami
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  2. K Inokuchi
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Inami, M., Inokuchi, K., Okabe, M. et al. Polycythemia associated with the JAK2V617F mutation emerged during treatment of chronic myelogenous leukemia. Leukemia 21, 1103–1104 (2007). https://doi.org/10.1038/sj.leu.2404591

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