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This Article Full Text (PDF) 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 Hayashi, Y. Articles by Williams, D. L. Search for Related Content PubMed PubMed Citation Articles by Hayashi, Y. Articles by Williams, D. L. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Two karyotypically independent leukemic clones with the t(8;21) and 11q23 translocation in acute myeloblastic leukemia at relapse [published erratum appears in Blood 1989 Aug 15;74(3):1180] Y Hayashi, SC Raimondi, FG Behm, VM Santana, DK Kalwinsky, CH Pui, J Mirro and DL Williams Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38101. Leukemic blast cells are thought to arise from clonal expansion of a single transformed hematopoietic cell. This generality is supported by the rarity of convincing reports on acute myeloblastic leukemia (AML) with two karyotypically independent clones. Relying on sequential cytogenetic analyses, we identified such clones in two children with relapsed AML. The first case, classified as M2 leukemia in the French- American-British (FAB) classification system, had a t(8;21) (q22;q22) at diagnosis; 16 months later, at relapse, the leukemic cells had uniform morphologic features similar to those observed at diagnosis, except that two independent clones were present: one with the original t(8;21) and the other with t(11;22)(q23;q13) [corrected]). The second case was initially classified as FAB M1 leukemia with a t(8;21) (q22;q22). At relapse, 16 months later, the blast cells appeared morphologically uniform and similar to the diagnostic specimen; however, in addition to the original t(8;21) clone, there was a t(1;11) (p32;q23) [corrected]. These findings suggest that separate leukemogenic events affecting different progenitor cells can occur in rare cases of AML. The presence of two karyotypically independent clones could also be explained by multistep leukemogenesis; that is, more than one cell from a common pool of preleukemic cells could be affected by the transforming event, resulting in two independent clones. Alternatively, in light of recent reports of therapy-related leukemias with an 11q23 translocation, the new independent clone in these two patients could represent a therapy-related secondary malignancy. Thus, 11q23 translocations may occur preferentially in stem cells that are more susceptible to treatment-induced malignant transformation. Volume 73, Issue 6, pp. 1650-1655, 05/01/1989 Copyright © 1989 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: A. Abe, N. Emi, M. Tanimoto, H. Terasaki, T. Marunouchi, and H. Saito Fusion of the Platelet-Derived Growth Factor Receptor beta  to a Novel Gene CEV14 in Acute Myelogenous Leukemia After Clonal Evolution Blood, December 1, 1997; 90(11): 4271 - 4277. [Abstract] [Full Text] [PDF]

	Copyright © 1989 by American Society of Hematology         Online ISSN: 1528-0020