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Blood, 1 October 2004, Vol. 104, No. 7, pp. 2163-2171. Prepublished online as a Blood First Edition Paper on June 22, 2004; DOI 10.1182/blood-2003-09-3033. This Article Full Text (PDF) All Versions of this Article: 2003-09-3033v1 104/7/2163    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 Pelletier, S. D Articles by Li, S. Search for Related Content PubMed PubMed Citation Articles by Pelletier, S. D Articles by Li, S. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 4, 2003 Accepted May 25, 2004 Lack of the adhesion molecules P-selectin and Intercellular adhesion molecule-1 accelerates the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice Shawn D Pelletier, Daniel S Hong, Yiguo Hu, Yuhua Liu, and Shaoguang Li* The Jackson Laboratory, Bar Harbor, Maine, USA Harvard University, Cambridge, Massachusetts, USA * Corresponding author; email: sli{at}jax.org. In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemogenesis. Using mice with homozygous inactivation of genes encoding the two adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced CML-like leukemia at a significantly faster rate than do wild-type mice. Lack of P-selectin and ICAM1 did not have a significant effect on the development of B-cell acute lymphoblstic leukemia (B-ALL) induced by BCR/ABL. Using mice deficient for P-selectin or ICAM1 alone, we show that P-selectin play a major role in the acceleration of CML-like leukemia. Lack of P-selectin resulted in early release of BCR/ABL-expressing myeloid progenitors from bone marrow, appearing to alter the biological properties of leukemic cells rather than their growth rate by increasing their homing to the lungs, causing fatal lung hemorrhages. These results indicate that adhesion of BCR/ABL-expressing myeloid progenitors to marrow stroma through P-selectin and ICAM1 plays an inhibitory role in the development of CML-like disease, suggesting that improvement of adhesion between BCR/ABL-expressing myeloid progenitor cells and bone marrow stroma may be of therapeutic value for human CML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Restraining CML by adhesives Ruibao Ren Blood 2004 104: 1917-1918. [Full Text] [PDF] This article has been cited by other articles: L. Kong, Y. Hu, C. Peng, Z. Wang, T. Duffy, A. Goodrich, and S. Li Increase in Leukemic Stem Cells Is Associated with Acceleration of BCR-ABL-Induced CML in P-Selectin-Deficient Mice. Blood (ASH Annual Meeting Abstracts), November 1, 2006; 108(11): 2129 - 2129. [Abstract] [PDF] M. Nieborowska-Skorska, G. Hoser, L. Rink, M. Malecki, P. Kossev, M. A. Wasik, and T. Skorski Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells. Cancer Res., April 15, 2006; 66(8): 4108 - 4116. [Abstract] [Full Text] [PDF]

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