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This Article Full Text Full Text (PDF) 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 Cooper, L. J. N. Articles by Sievers, E. L. Search for Related Content PubMed PubMed Citation Articles by Cooper, L. J. N. Articles by Sievers, E. L. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents Blood, 15 September 2000, Vol. 96, No. 6, pp. 2310-2313 BRIEF REPORT Evidence that juvenile myelomonocytic leukemia can arise from a pluripotential stem cell Laurence J. N. Cooper, Kevin M. Shannon, Michael R. Loken, Molly Weaver, Karen Stephens, and Eric L. Sievers From the Departments of Pediatrics, Medicine, and Laboratory Medicine, University of Washington, and Hematologics, Inc, Seattle WA; and the Department of Pediatrics, University of California, San Francisco, CA. Children with neurofibromatosis type 1 (NF1) carry germline mutations in one allele of the NF1 gene and are predisposed to myeloid malignancies, particularly juvenile myelomonocytic leukemia (JMML). Disruption of the remaining NF1 allele can be found in malignant cells. Flow cytometric cell sorting techniques to isolate the malignant cell populations and molecular genetic methods to assay for somatic loss of the normal NF1 allele were used to study an unusual child with NF1 and JMML who subsequently had T-cell lymphoma. The data show that malignant JMML and lymphoma cells share a common loss of genetic material involving the normal NF1 gene and approximately 50 Mb of flanking sequence, suggesting that the abnormal T-lymphoid and myeloid populations were derived from a common precursor cell. These data support the hypothesis that JMML can arise in a pluripotent hematopoietic cell. © 2000 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: D. T. Le, N. Kong, Y. Zhu, J. O. Lauchle, A. Aiyigari, B. S. Braun, E. Wang, S. C. Kogan, M. M. Le Beau, L. Parada, et al. Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder Blood, June 1, 2004; 103(11): 4243 - 4250. [Abstract] [Full Text] [PDF] D. A. Ingram, L. Zhang, J. McCarthy, M. J. Wenning, L. Fisher, F.-C. Yang, D. W. Clapp, and R. Kapur Lymphoproliferative defects in mice lacking the expression of neurofibromin: functional and biochemical consequences of Nf1 deficiency in T-cell development and function Blood, November 15, 2002; 100(10): 3656 - 3662. [Abstract] [Full Text] [PDF] V. I. Rebel, A. L. Kung, E. A. Tanner, H. Yang, R. T. Bronson, and D. M. Livingston Distinct roles for CREB-binding protein and p300 in hematopoietic stem cell self-renewal PNAS, November 12, 2002; 99(23): 14789 - 14794. [Abstract] [Full Text] [PDF] R. J. Arceci, B. J. Longley, and P. D. Emanuel Atypical Cellular Disorders Hematology, January 1, 2002; 2002(1): 297 - 314. [Abstract] [Full Text]

	Copyright © 2000 by American Society of Hematology         Online ISSN: 1528-0020