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Advances in HematologyVolume 2012 2012, Article ID 535709, 6 pages

Review ArticleDepartment of Hematology, Erasmus University Medical Center, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands

Received 12 September 2011; Revised 29 November 2011; Accepted 4 December 2011

Academic Editor: Mark R. Litzow

Copyright © 2012 Mar Bellido and Peter A. W. te Boekhorst. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

JAK2 is a tyrosine kinase gene that plays an essential role in the development of normal haematopoiesis. Hyperactivation of JAK2 occurs in myeloproliferative neoplasms by different mechanisms. As a consequence, JAK2 inhibitors have been designed to suppress the cytokine signalling cascade caused by the constitutive activation of JAK2. In clinical trials, JAK2 inhibitors are efficient in decreasing spleen size, controlling clinical symptoms, and improving quality of life in patients with myeloproliferative neoplasms. However, JAK2 inhibitors are unable to target uncommitted hematopoietic progenitors responsible of the initiation of the myeloproliferative disease. It is expected that, in order to cure the myeloproliferative disease, JAK2 inhibitors should be combined with other drugs to target simultaneously different pathways and to target the initiator hematopoietic cell population in myeloproliferative disorders. Taking advantage of the inhibition of the cytokine cascade of JAK2 inhibitors, these compounds are going to be used not only to treat patients with hematological neoplasms but may also be beneficial to treat patients with rheumatoid arthritis or other inflammatory diseases.





Autor: Mar Bellido and Peter A. W. te Boekhorst

Fuente: https://www.hindawi.com/



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