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Blood, 1 October 2009, Vol. 114, No. 14, pp. 3127-3130. Prepublished online as a Blood First Edition Paper on July 23, 2009; DOI 10.1182/blood-2008-12-190991.
VASCULAR BIOLOGY Endothelial colony-forming cells from patients with chronic myeloproliferative disorders lack the disease-specific molecular clonality marker![]() ![]() 1 Divisione Ematologia, Ospedale San Martino, Genova; 2 Laboratory of Organ Transplantation, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Matteo Foundation, Pavia; 3 Centro Cellule Staminali e Terapia Cellulare, Ospedale San Martino, Genova; 4 Medicina Interna ed Oncologia Medica, IRCCS Fondazione Policlinico San Matteo, Pavia; 5 Unit of Clinical Epidemiology-Center for the Study of Myelofibrosis, IRCCS Policlinico San Matteo Foundation, Pavia; 6 Dipartimento Genetica Umana, University of Pavia, Pavia; 7 Laboratorio Diagnostica Emato-Oncologica, Biomolecolare e Citogenetica, Dipartimento Medicina Intema, Università di Genova, Genova; 8 Laboratorio Terapie Cellulari, Dipartimento Medicina Intema, Università di Genova, Genoa; 9 Laboratory of Biotechnology, IRCCS Policlinico San Matteo Foundation, Pavia; 10 Clinica di Medicina Interna 3, Ospedale San Martino, Genoa; 11 Dipartimento di Medicina Interna, Universita'di Pavia IRCCS Fondazione Policlinico San Matteo, Pavia; and 12 Immunoemathology and Transfusion Service, IRCCS Policlinico San Matteo Foundation, Pavia, Italy
Two putative types of circulating endothelial progenitor cells have been recently identified in vitro: (1) endothelial colony-forming cell (ECFC) and (2) colony-forming unit–endothelial cell (CFU-EC). Only the former is now recognized to belong to endothelial lineage. We have used the ECFC and CFU-EC assays to readdress the issue of the clonal relation between endothelial progenitor cells and hematopoietic stem cells in patients with Philadelphia-positive and Philadelphia-negative chronic myeloproliferative disorders. Both ECFCs and CFU-ECs were cultured from peripheral blood mononuclear cells, and either BCR-ABL rearrangement or JAK2-V617F mutation were assessed in both types of endothelial colonies. We found that ECFCs lack the disease-specific markers, which are otherwise present in CFU-ECs, thus reinforcing the concept that the latter belongs to the hematopoietic lineage, and showing that in chronic myeloproliferative disorders the cell that gives rise to circulating ECFC has a distinct origin from the cell of the hematopoietic malignant clone.
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