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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2688-2692. Prepublished online as a Blood First Edition Paper on November 28, 2006; DOI 10.1182/blood-2006-07-021980. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-07-021980v1 109/7/2688    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 Flynn, C. M. Articles by Kaufman, D. S. Search for Related Content PubMed PubMed Citation Articles by Flynn, C. M. Articles by Kaufman, D. S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Neoplasia Stem Cells in Hematology Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PERSPECTIVE Donor cell leukemia: insight into cancer stem cells and the stem cell niche Catherine M. Flynn1, and Dan S. Kaufman1 1 Stem Cell Institute and Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, MN Donor cell leukemia (DCL) is a rare complication of hematopoietic cell transplantation (HCT). Its incidence has been reported between 0.12% and 5%, although the majority of cases are anecdotal. The mechanisms of leukemogenesis in DCL may be distinct from other types of leukemia. Possible causes of DCL include oncogenic alteration or premature aging of transplanted donor cells in an immunosuppressed person. Although many studies have recently better characterized leukemic stem cells, it is important to also consider that both intrinsic cell factors and external signals from the hematopoietic microenvironment govern the developmental fate of hematopoietic stem cells (HSCs). Therefore, in cases of DCL, alteration of the microenvironment after HCT may increase the likelihood that some progeny of normal HSCs become leukemic. This complex intercommunication between cells, growth factors, and cytokines in the hematopoietic microenvironment are critical to balance HSC self-renewal, proliferation, and differentiation. However, this homeostasis is likely perturbed in the development of DCL, allowing unique insight into the stimuli that regulate normal and potentially abnormal hematopoietic development. In this article, we discuss the possible pathogenesis of DCL, its association with stem cells, and its likely dependence on a less-supportive stem cell niche. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Development of original donor cell leukemia after successful engraftment from a second donor Jane M. Stevens, Denise Syndercombe-Court, Heather E. Oakervee, Daniel McCloskey, Michael J. Jenner, John G. Gribben, and Jamie D. Cavenagh Blood 2007 110: 4621-4622. [Full Text] [PDF] This article has been cited by other articles: J. M. Stevens, D. Syndercombe-Court, H. E. Oakervee, D. McCloskey, M. J. Jenner, J. G. Gribben, and J. D. Cavenagh Development of original donor cell leukemia after successful engraftment from a second donor Blood, December 15, 2007; 110(13): 4621 - 4622. [Full Text] [PDF]

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