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 Blood, 21 May 2009, Vol. 113, No. 21, pp. 5246-5249.
Prepublished online as a Blood First Edition Paper on March 17, 2009; DOI 10.1182/blood-2008-11-191544.

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MYELOID NEOPLASIA

Brief report

The presence of JAK2V617F mutation in the liver endothelial cells of patients with Budd-Chiari syndrome

Selcuk Sozer1,2, Maria Isabel Fiel3, Thomas Schiano4, Mingjiang Xu1,5, John Mascarenhas1,5, and Ronald Hoffman1,5

1 Tisch Cancer Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY; 2 Uludag University School of Medicine, Bursa, Turkey; 3 Department of Pathology and 4 Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY; and 5 Myeloproliferative Disorder Research Consortium, New York, NY

Patients with myeloproliferative disorders are at a high risk of developing thrombotic events. Several investigators have hypothesized that endothelial cell (EC) abnormalities might contribute to this prothrombotic state. Budd-Chiari syndrome (BCS) and portal vein thrombosis have been reported to be associated with JAK2V617F-positive hematopoiesis. We explored whether JAK2V617F was present in ECs in the vessels of polycythemia vera (PV) patients with BCS using laser capture microdissection followed by nested polymerase chain reaction or reverse-transcribed polymerase chain reaction. The ECs of the 2 BCS patients with PV were homozygous for the JAK2V617F and were shown to express transcripts characteristic of ECs but not hematopoietic cells. ECs of the other BCS patient with PV and 2 patients with hepatoportal sclerosis without PV contained exclusively wild-type JAK2. The presence of JAK2V617F in both ECs and hematopoietic cells belonging to BCS patients with PV indicate that ECs in PV are involved by the malignant process and that in a subpopulation of the patients the disease might originate from a common cell of origin for hematopoietic and ECs.


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F. Cervantes, E. Arellano-Rodrigo, and A. Alvarez-Larran
Blood cell activation in myeloproliferative neoplasms
Haematologica, November 1, 2009; 94(11): 1484 - 1488.
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