A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

Chloé James, Valérie Ugo, Jean-Pierre Le Couédic, Judith Staerk, François Delhommeau, Catherine Lacout, Loïc Garçon, Hana Raslova, Roland Berger, Annelise Bennaceur-Griscelli, Jean Luc Villeval, Stefan N. Constantinescu, Nicole Casadevall and William Vainchenker ()
Additional contact information
Chloé James: Paris XI University
Valérie Ugo: Paris XI University
Jean-Pierre Le Couédic: Paris XI University
Judith Staerk: Université Catholique de Louvain
François Delhommeau: Paris XI University
Catherine Lacout: Paris XI University
Loïc Garçon: Paris XI University
Hana Raslova: Paris XI University
Roland Berger: Hôpital Necker
Annelise Bennaceur-Griscelli: Paris XI University
Jean Luc Villeval: Paris XI University
Stefan N. Constantinescu: Université Catholique de Louvain
Nicole Casadevall: Paris XI University
William Vainchenker: Paris XI University

Nature, 2005, vol. 434, issue 7037, 1144-1148

Abstract: Polycythaemia vera The basis of the bone marrow abnormality in polycythaemia vera, a blood disorder often linked to leukaemia, has finally been identified. Over 80% of patients have a mutation in the JAK2 enzyme; this normally stimulates red blood cell production when needed, after blood loss for example. The mutant enzyme is permanently in the ‘on’ position. The JAK2 mutation was also found in several other myeloproliferative disorders. With JAK2 as a possible target, it may be possible to develop targeted therapies similar to Glivec, now used to treat chronic myeloid leukaemia.

Date: 2005
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DOI: 10.1038/nature03546

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