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Prepublished online as a Blood First Edition Paper on December 27, 2002; DOI 10.1182/blood-2002-08-2383. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-08-2383v1 101/9/3568    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 Lentzsch, S. Articles by Mapara, M. Y. Search for Related Content PubMed PubMed Citation Articles by Lentzsch, S. Articles by Mapara, M. Y. Related Collections Immunobiology Neoplasia Apoptosis Cell Adhesion and Motility Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 May 2003, Vol. 101, No. 9, pp. 3568-3573 IMMUNOBIOLOGY Macrophage inflammatory protein 1-alpha (MIP-1) triggers migration and signaling cascades mediating survival and proliferation in multiple myeloma (MM) cells Suzanne Lentzsch, Margarete Gries, Martin Janz, Ralf Bargou, Bernd Dörken, and Markus Y. Mapara From the University Medical Center Charite, Department of Hematology, Oncology and Tumorimmunology, Robert-Rössle-Klinik, Campus Buch; and Campus Virchow Klinikum, Humboldt University, Berlin, Germany. Recently, it has been demonstrated that macrophage inflammatory protein 1- alpha (MIP-1) is crucially involved in the development of osteolytic bone lesions in multiple myeloma (MM). The current study was designed to determine the direct effects of MIP-1 on MM cells. Thus, we were able to demonstrate that MIP-1 acts as a potent growth, survival, and chemotactic factor in MM cells. MIP-1-induced signaling involved activation of the AKT/protein kinase B (PKB) and the mitogen-activated protein kinase (MAPK) pathway. In addition, inhibition of AKT activation by phosphatidylinositol 3- kinase (PI3-K) inhibitors did not influence MAPK activation, suggesting that there is no cross talk between MIP-1-dependent activation of the PI3-K/AKT and extracellular-regulated kinase (ERK) pathway. Our data suggest that besides its role in development of osteolytic bone destruction, MIP-1 also directly affects cell signaling pathways mediating growth, survival, and migration in MM cells and provide evidence that MIP-1 might play a pivotal role in the pathogenesis of MM. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: O. Sezer Myeloma Bone Disease: Recent Advances in Biology, Diagnosis, and Treatment Oncologist, March 1, 2009; 14(3): 276 - 283. [Abstract] [Full Text] [PDF] S. Vallet, N. Raje, K. Ishitsuka, T. Hideshima, K. Podar, S. Chhetri, S. Pozzi, I. Breitkreutz, T. Kiziltepe, H. Yasui, et al. MLN3897, a novel CCR1 inhibitor, impairs osteoclastogenesis and inhibits the interaction of multiple myeloma cells and osteoclasts Blood, November 15, 2007; 110(10): 3744 - 3752. [Abstract] [Full Text] [PDF] S. T. Pals, D. J. J. de Gorter, and M. 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