Altered gene expression in myeloproliferative disorders correlates with activation of signaling by the V617F mutation of Jak2

被引:136
作者
Kralovics, R
Teo, SS
Buser, AS
Brutsche, M
Tiedt, R
Tichelli, A
Passamonti, F
Pietra, D
Cazzola, M
Skoda, RC
机构
[1] Univ Basel Hosp, Dept Res, Div Clin Hematol, CH-4031 Basel, Switzerland
[2] Univ Basel Hosp, Div Pneumol, CH-4031 Basel, Switzerland
[3] Univ Basel Hosp, Div Diagnost Hematol, CH-4031 Basel, Switzerland
[4] Univ Pavia, Sch Med, Div Hematol, I-27100 Pavia, Italy
[5] Policlin San Matteo, IRCCS, Pavia, Italy
关键词
D O I
10.1182/blood-2005-05-1889
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We identified 13 new gene expression markers that were elevated and one marker, ANKRD15, that was down-regulated in patients with polycythemia vera (PV). These 14 markers, as well as the previously described PRV1 and NF-E2, exhibited the same gene expression alterations also in patients with exogenously activated granulocytes due to sepsis or granulocyte colony-stimulating factor (G-CSF) treatment. The recently described V617F mutation in the Janus kinase 2 (JAK2) gene allows defining subclasses of patients with myeloproliferative disorders based on the JAK2 genotype. Patients with PV who were homozygous or heterozygous for JAK2-V617F exhibited higher levels of expression of the 13 new markers, PRV1, and NF-E2 than patients without JAK2-V617F, whereas ANKRD15 was down-regulated in these patients. Our results suggest that the alterations in expression of the markers studied are due to the activation of the Jak/signal transducer and activator of transcription (STAT) pathway through exogenous stimuli (sepsis or G-CSF treatment), or endogenously through the JAK2-V617F mutation.
引用
收藏
页码:3374 / 3376
页数:3
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