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JAK the trigger

Oncogene volume 24, pages 7125–7126 (2005)Cite this article

Abstract

A somatic mutation that leads to activation of the JAK2 tyrosine kinase has recently been identified as a recurrent genetic abnormality in several different myeloproliferative disorders. A translocation generating the constitutively activated fusion protein PCM1-JAK2 has also been recently found in atypical chronic myelogenous leukemia and acute leukemia. This recent spate of independent studies (one of which is published in this issue of Oncogene) establish abnormal JAK2 activation as the underlying defect in a significant number of cases of myeloproliferative disease, and JAK2 as an important new therapeutic target.

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  1. Laboratoire d'hématopoïèse leucémique et cible thérapeutique, Université Victor Segalen Bordeaux 2, Service des maladies du sang CHU de Bordeaux, INSERM E0217, 146 rue Léo Saignat, Boite 50, 33076, Bordeaux Cedex, France

    François-Xavier Mahon

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Correspondence to François-Xavier Mahon.

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Mahon, FX. JAK the trigger. Oncogene 24, 7125–7126 (2005). https://doi.org/10.1038/sj.onc.1208885

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