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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.
 Previous Article | Next Article 
Submitted October 13, 2005
Accepted April 21, 2006
Constitutive activation of STAT5 and Bcl-xL overexpression
can induce endogenous erythroid colony formation in human
primary cells
Loic Garcon, Christine Rivat, Chloe James, Catherine Lacout, Valerie Camara-Clayette, Valerie Ugo, Yann Lecluse, Annelise Bennaceur-Griscelli, and William Vainchenker*
U 790 INSERM, Institut Gustave Roussy, 39 rue Camille Desmoulins, 94805 Villejuif, France
IFR 54, Institut Gustave Roussy, 39 rue Camille Desmoulins, 94805 Villejuif, France
* Corresponding author; email: verpre{at}igr.fr.
The biological hallmark of PV is the formation of
endogenous erythroid colonies (EEC) with an
erythropoietin-independent erythroid 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
CFU-E formation in the presence of Epo. Altogether these
results demonstrate that a sustained level of the sole
Bcl-xL is capable to give 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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