Leukemia Research
Volume 33, Issue 12 , Pages 1581-1583, December 2009

How do JAK2-inhibitors work in myelofibrosis: An alternative hypothesis

  • Alessandro M. Vannucchi

      Affiliations

    • Corresponding Author InformationCorrespondence address: Department of Hematology, University of Florence, Viale Morgagni 85, 50134 Florence, Italy. Tel.: +39 055 7947 688; fax: +39 055 7947 688.

UF of Hematology, Department of Critical care, University of Florence, Florence, Italy

Received 3 June 2009; received in revised form 3 June 2009; accepted 3 June 2009. published online 07 March 2011.

Abstract 

The clinical efficacy of JAK2-inhibitors in patients with myelofibrosis, that involves a rapid and massive reduction of spleen enlargement and improvement of clinical symptoms, is not accompanied by significant modifications of hematologic parameters nor of the burden of JAK2V617F allele. Furthermore, clinical improvement has been reported to occur irrespective of patient's JAK2-mutated status. On the other hand, dramatic changes in plasma cytokine levels have been observed. Based on available information about the role of cytokines in the pathogenesis of myelofibrosis, the hypothesis that the clinical efficacy of JAK2-inhibitors could be mainly ascribed to a general down-regulation of cytokine production and cytokine signaling is discussed.

Keywords: JAK2, JAK2-inhibitor, Myelofibrosis, Cytokine

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PII: S0145-2126(09)00281-1

doi:10.1016/j.leukres.2009.06.001

Leukemia Research
Volume 33, Issue 12 , Pages 1581-1583, December 2009

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