SEARCH:   Advanced

Blood, 2 April 2009, Vol. 113, No. 14, pp. 3287-3296. Prepublished online as a Blood First Edition Paper on January 15, 2009; DOI 10.1182/blood-2008-04-154187. This Article Full Text Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2008-04-154187v1 113/14/3287    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 Cox, C. V. Articles by Blair, A. Search for Related Content PubMed PubMed Citation Articles by Cox, C. V. Articles by Blair, A. Related Collections Lymphoid Neoplasia Related Articles in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  LYMPHOID NEOPLASIA Expression of CD133 on leukemia-initiating cells in childhood ALL Charlotte V. Cox1,2, Paraskevi Diamanti1,2, Roger S. Evely3, Pamela R. Kearns4, and Allison Blair1,2 1 Bristol Institute for Transfusion Sciences, Bristol; 2 Department of Cellular and Molecular Medicine, University of Bristol, Bristol; 3 Bristol Haematology and Oncology Centre, Bristol; and 4 Division of Reproductive and Child Health, University of Birmingham, Birmingham, United Kingdom Optimization of therapy for childhood acute lymphoblastic leukemia (ALL) requires a greater understanding of the cells that proliferate to maintain this malignancy because a significant number of cases relapse, resulting from failure to eradicate the disease. Putative ALL stem cells may be resistant to therapy and subsequent relapses may arise from these cells. We investigated expression of CD133, CD19, and CD38 in pediatric B-ALL. Cytogenetic and molecular analyses demonstrated that karyotypically aberrant cells were present in both CD133+/CD19+ and CD133+/CD19– subfractions, as were most of the antigen receptor gene rearrangements. However, ALL cells capable of long-term proliferation in vitro and in vivo were derived from the CD133+/CD19– subfraction. Moreover, these CD133+/CD19– cells could self-renew to engraft serial nonobese diabetic–severe combined immunodeficient recipients and differentiate in vivo to produce leukemias with similar immunophenotypes and karyotypes to the diagnostic samples. Furthermore, these CD133+/CD19– ALL cells were more resistant to treatment with dexamethasone and vincristine, key components in childhood ALL therapy, than the bulk leukemia population. Similar results were obtained using cells sorted for CD133 and CD38, with only the CD133+/CD38– subfraction demonstrating xenograft repopulating capacity. These data suggest that leukemia-initiating cells in childhood B-ALL have a primitive CD133+/CD19– and CD38– phenotype. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Articles in Blood Online: Malignant stem cells in childhood ALL: the debate continues! Olaf Heidenreich and Josef Vormoor Blood 2009 113: 4476-4477. [Full Text] [PDF] Stem cells in childhood acute lymphoblastic leukemia: identifying the most relevant targets for therapy Paraskevi Diamanti and Allison Blair Blood 2009 113: 4477. [Full Text] [PDF] This article has been cited by other articles: O. Heidenreich and J. Vormoor Malignant stem cells in childhood ALL: the debate continues! Blood, April 30, 2009; 113(18): 4476 - 4477. [Full Text] [PDF] P. Diamanti and A. Blair Stem cells in childhood acute lymphoblastic leukemia: identifying the most relevant targets for therapy Blood, April 30, 2009; 113(18): 4477 - 4477. [Full Text] [PDF]

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020