SEARCH:   Advanced

Download ALL Selected Citations to Citation Manager Selected Abstracts Returned: 1 citations and abstracts. Click on down arrow or scroll to see abstracts. Shawn D Pelletier, Daniel S Hong, Yiguo Hu, Yuhua Liu, and Shaoguang Li 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 Blood First Edition Paper, prepublished online June 22, 2004; DOI 10.1182/blood-2003-09-3033 Blood, 22 June 2004, Vol. 0, No. 2004, pp. 200309303. Abstract 1 of 1 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. [Reprint (PDF) Version of Pelletier et al.]

	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020