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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1575-1583. Prepublished online as a Blood First Edition Paper on October 30, 2007; DOI 10.1182/blood-2007-09-114231. This Article Full Text Full Text (PDF) Supplemental Appendix, Tables, and Figures All Versions of this Article: blood-2007-09-114231v1 111/3/1575    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Forestier, E. Articles by Johansson, B. Search for Related Content PubMed PubMed Citation Articles by Forestier, E. Articles by Johansson, B. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study Erik Forestier1, Shai Izraeli2, Berna Beverloo3, Oskar Haas4, Andrea Pession5, Kyra Michalová6, Batia Stark7, Christine J. Harrison8, Andrea Teigler-Schlegel9, and Bertil Johansson10 1 Pediatrics Unit, Department of Clinical Sciences, University of Umeå, Umeå, Sweden; 2 Department of Pediatric Hemato-Oncology, Cancer Research Center, Safra's Children's Hospital, Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel; 3 Department of Clinical Genetics, Erasmus Medical Center, Rotterdam, the Netherlands; 4 Department of Pediatric Hematology and Oncology and Children's Cancer Research Institute, St Anna Children's Hospital, Vienna, Austria; 5 Department of Pediatrics, University of Bologna, San Orsola Hospital, Bologna, Italy; 6 Center of Oncocytogenetics Institute of Clinical Biochemistry and Laboratory Diagnostics, General Faculty Hospital and 1st Medical Faculty, Charles University, Prague, Czech Republic; 7 Department of Pediatric Hematology/Oncology, Schneider Children's Medical Center of Israel, Petah Tikva, Israel; 8 Leukaemia Research Cytogenetics Group, Cancer Sciences Division, University of Southampton, Southampton, United Kingdom; 9 Oncogenetic Laboratory, Department of Human Genetics, Giessen, Germany; and 10 Department of Clinical Genetics, Lund University Hospital, Lund, Sweden Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these leukemias, we analyzed 215 DS-ALLs and 189 DS-AMLs. Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%). The HeH DS-ALLs were characterized by gains of the same chromosomes as non–DS-HeH, suggesting the same etiology/pathogenesis. In addition, specific genetic subtypes of DS-ALL were suggested by the significant overrepresentation of cases with +X, t(8;14)(q11;q32), and del(9p). Unlike DS-ALL, the common translocations associated with non–DS-AML were rare in DS-AML, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21. This series of DS leukemias—the largest to date—reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities. Furthermore, this analysis confirms that DS-AML is a distinct entity, originating through other genetic pathways than do non–DS-AMLs, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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