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Blood, 15 June 2005, Vol. 105, No. 12, pp. 4813-4819. Prepublished online as a Blood First Edition Paper on February 24, 2005; DOI 10.1182/blood-2004-10-4054. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-4054v1 105/12/4813    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Till, K. J. Articles by Cawley, J. C. Search for Related Content PubMed PubMed Citation Articles by Till, K. J. Articles by Cawley, J. C. Related Collections Cell Adhesion and Motility Signal Transduction Chemokines, Cytokines, and Interleukins Hemostasis, Thrombosis, and Vascular Biology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA CLL, but not normal, B cells are dependent on autocrine VEGF and 41 integrin for chemokine-induced motility on and through endothelium Kathleen J. Till, David G. Spiller, Robert J. Harris, Haijuan Chen, Mirko Zuzel, and John C. Cawley From the Department of Haematology, Duncan Building, Daulby Street; and Centre for Cell Imaging, Life Sciences Building, Crown Street, University of Liverpool, United Kingdom. Vascular endothelial cell growth factor (VEGF) is a multifunctional cytokine involved in tumor formation. In chronic lymphocytic leukemia (CLL), it is known that the malignant cells secrete VEGF and possess VEGF receptors. This suggests that an autocrine loop might be important in the pathogenesis of CLL. Here we show that, in patients with lymphadenopathy, autocrine VEGF and 41 integrin are involved in the chemokine-dependent motility of CLL cells on and through endothelium—processes important for the invasion of lymphoreticular tissues, a major determinant of disease outcome. In contrast, normal lymphocytes were not dependent on autocrine VEGF or 41 for either type of cell movement. Moreover, in contrast to normal B lymphocytes, CLL cells failed to cluster and activate L2 in response to chemokines, unless VEGF receptor(s) and 41 were also engaged by their respective ligands. This is the first demonstration that autocrine VEGF is involved in CLL-cell motility, and that the L2 on the malignant cells is functionally altered compared with that of normal B cells in not undergoing activation in response to chemokine alone. Given the importance of cell motility for tissue invasion, the present results provide a rationale for a trial of VEGF and 4 blockade in patients with CLL who have tissue disease. (Blood. 2005;105:4813-4819) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Redondo-Munoz, E. Ugarte-Berzal, J. A. Garcia-Marco, M. H. del Cerro, P. E. Van den Steen, G. Opdenakker, M. J. Terol, and A. Garcia-Pardo {alpha}4{beta}1 integrin and 190-kDa CD44v constitute a cell surface docking complex for gelatinase B/MMP-9 in chronic leukemic but not in normal B cells Blood, July 1, 2008; 112(1): 169 - 178. [Abstract] [Full Text] [PDF] P. E. M. Patten, A. G. S. Buggins, J. Richards, A. Wotherspoon, J. Salisbury, G. J. Mufti, T. J. Hamblin, and S. Devereux CD38 expression in chronic lymphocytic leukemia is regulated by the tumor microenvironment Blood, May 15, 2008; 111(10): 5173 - 5181. [Abstract] [Full Text] [PDF] T. 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