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Blood, 15 July 2004, Vol. 104, No. 2, pp. 495-501.
Prepublished online as a Blood First Edition Paper on February 19, 2004; DOI 10.1182/blood-2003-08-2695.
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NEOPLASIA
Imatinib mesylate (STI571) decreases the vascular endothelial growth factor plasma concentration in patients with chronic myeloid leukemia
Laurence Legros,
Christine Bourcier,
Arnaud Jacquel,
François-Xavier Mahon,
Jill-Patrice Cassuto,
Patrick Auberger, and
Gilles Pagès
From the Service d'Hématologie, Hôpital Archet, Nice, France; Unité Mixte de Recherche (UMR) 6543 Centre National de la Recherche Scientifique (CNRS)-UNSA (Université de Nice Sophia-Antipolis), Signaling, Developmental Biology and Cancer, Centre Antoine Lacassagne, Nice, France; Institut National de la Santé et de la Recherche Médicale (INSERM) U 526, Physiopathologie de la Survie et de la Mort Cellulaires, Institut Federatif de Recherche (IFR 50), Faculté de Médecine, Nice, France; and Laboratoire Greffe de Moelle, Université Victor Segalen, Bordeaux, France.
Increased angiogenesis in bone marrow (BM) is one of the characteristics of chronic myeloid leukemia (CML), a clonal myeloproliferative disorder that expresses a chimeric Bcr/Abl protein. Recently, the therapeutic strategy in CML has been totally modified with the development of a new drug: imatinib mesylate (STI571), a specific inhibitor of Bcr/Abl tyrosine kinase activity. The aim of our study was to determine, in patients with CML, the capacity of imatinib mesylate to modulate one of the most potent regulators of angiogenesis, the vascular endothelial growth factor (VEGF). In newly diagnosed CML, we observed significantly increased VEGF secretion by CML BM cells and significantly increased VEGF plasma concentrations. We showed that low plasma VEGF concentrations could be one of the characteristics of complete cytogenetic remission. To understand the molecular mechanisms leading to the inhibition of VEGF production by imatinib, we focused our experiments on the human cell line K562, which is Bcr/Abl positive. We demonstrated that imatinib inhibits VEGF gene transcription by targeting the Sp1 and Sp3 transcription factors. Taken together, our results highlight the potential prognostic value of VEGF concentrations in evaluating the evolution of CML patients treated with imatinib. (Blood. 2004;104: 495-501)
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