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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. This Article Full Text (PDF) All Versions of this Article: 2003-08-2695v1 104/2/495    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Legros, L. Articles by Pages, G. Search for Related Content PubMed PubMed Citation Articles by Legros, L. Articles by Pages, G. Social Bookmarking                   What's this? Submitted August 7, 2003 Accepted February 1, 2004 Imatinib Mesylate (STI571) decreases the Vascular Endothelial Growth Factor plasma level in patients with Chronic Myeloid Leukemia Laurence Legros*, Christine Bourcier, Arnaud Jacquel, Francois-Xavier Mahon, Jill-Patrice Cassuto, Patrick Auberger, and Gilles Pages Service d'Hematologie, Hopital Archet 1, Nice, France; Signaling Developmental Biology and Cancer, CNRS UMR 6543, Nice, France Signaling Developmental Biology and Cancer, CNRS UMR 6543, Nice, France Physiologie de la Survie et de la Mort Cellulaires, INSERM U 526, Nice, France Laboratoire Greffe de Moelle, Universite Victor Segalen, Bordeaux, France Service d'Hematologie, Hopital Archet 1, Nice, France * Corresponding author; email: legros{at}unice.fr. Increased angiogenesis in bone marrow (BM) is one of the characteristics of chronic myeloid leukemia (CML), a clonal myeloproliferative disorder which 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 levels. We showed that low plasma VEGF levels 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 levels in evaluating the evolution of CML patients treated with Imatinib. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. H. Kim, W. Xu, S. Kamel-Reid, X. Liu, C. W. Jung, S. Kim, and J. H. Lipton Clinical relevance of vascular endothelial growth factor (VEGFA) and VEGF receptor (VEGFR2) gene polymorphism on the treatment outcome following imatinib therapy Ann. Onc., October 29, 2009; (2009) mdp452v1. [Abstract] [Full Text] [PDF] N. Y. Tan and L. M. Khachigian Sp1 Phosphorylation and Its Regulation of Gene Transcription Mol. Cell. Biol., May 15, 2009; 29(10): 2483 - 2488. [Full Text] [PDF] Y. Gao, A. Howard, K. Ban, and J. Chandra Oxidative Stress Promotes Transcriptional Up-regulation of Fyn in BCR-ABL1-expressing Cells J. Biol. Chem., March 13, 2009; 284(11): 7114 - 7125. [Abstract] [Full Text] [PDF] D. H. Kim, W. Xu, C. 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