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 Blood, 1 September 2006, Vol. 108, No. 5, pp. 1551-1554.
Prepublished online as a Blood First Edition Paper on May 9, 2006; DOI 10.1182/blood-2005-10-009514.

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HEMATOPOIESIS
Brief report

Constitutive activation of STAT5 and Bcl-xL overexpression can induce endogenous erythroid colony formation in human primary cells

Loïc Garçon, Christine Rivat, Chloé James, Catherine Lacout, Valérie Camara-Clayette, Valérie Ugo, Yann Lecluse, Annelise Bennaceur-Griscelli, and William Vainchenker

From the Unité (U) 790 Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Gustave Roussy, Villejuif, France; Laboratoire d'Hématologie, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France; and Laboratoire d'Hématologie, Centre Hospitalo-Universitaire (CHU) de Brest-Hôpital Morvan, Institut Gustave Roussy, Villejuif, France.

The biologic hallmark of polycythemia vera (PV) is the formation of endogenous erythroid colonies (EECs) with an erythropoietin-independent differentiation. Recently, it has been shown that an activating mutation of JAK2 (V617F) was at the origin of PV. In this work, we studied whether the STAT5/Bcl-xL pathway could be responsible for EEC formation. A constitutively active form of STAT5 was transduced into human erythroid progenitors and induced an erythropoietin-independent terminal differentiation and EEC formation. Furthermore, Bcl-xL overexpression in erythroid progenitors was also able to induce erythroid colonies despite the absence of erythropoietin. Conversely, siRNA-mediated STAT5 and Bcl-xL knock-down in human erythroid progenitors inhibited colony-forming unit-erythroid (CFU-E) formation in the presence of Epo. Altogether, these results demonstrate that a sustained level of the sole Bcl-xL is capable of giving rise to Epo-independent erythroid colony formation and suggest that, in PV patients, JAK2V617F may induce EEC via the STAT5/Bcl-xL pathway.


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