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Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden, Department of Clinical Genetics, University Hospital, SE-221 85 Lund, Sweden.
Mörse, H., Department of Pediatrics, Lund University Hospital, Lund, Sweden.
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden.
Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
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2005 (English)In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 44, no 2, 113-122 p.Article in journal (Refereed) Published
Abstract [en]

High hyperdiploidy (>50 chromosomes) in childhood acute lymphoblastic leukemia (ALL) is characterized by nonrandom multiple trisomies and tetrasomies involving in particular chromosomes X, 4, 6, 8, 10, 14, 17, 18, and 21. This characteristic karyotypic pattern, the most common in pediatric ALL, may arise via a tetraploid state with subsequent loss of chromosomes, by sequential gains of chromosomes in consecutive cell divisions, or by simultaneous gain of chromosomes in a single mitosis. These alternatives may be distinguished by investigation of the allelic ratios of loci on the tetrasomic and disomic chromosomes. Previous studies of tetrasomy 21 and of the occurrence of uniparental disomies (UPDs) have suggested that the most likely mechanism is simultaneous gain. However, the other pathways have not been definitely excluded because complete analyses of all disomies and tetrasomies have never been performed. In the present study, we investigated 27 hyperdiploid ALLs by using 58 polymorphic microsatellite markers mapped to 23 of the 24 human chromosomes. Twenty-six tetrasomies were analyzed (involving chromosomes X, 8, 10, 14, 18, and 21), and the frequency of UPDs was determined in 10 cases. In total, 200 chromosomes were studied. Equal allele dosage was observed in 24 of 26 tetrasomies, and only 7 UPDs were found. These data strongly suggest that hyperdiploidy in childhood ALL generally arises by a simultaneous gain of all additional chromosomes in a single abnormal mitosis. © 2005 Wiley-Liss, Inc.

Place, publisher, year, edition, pages
2005. Vol. 44, no 2, 113-122 p.
National Category
Natural Sciences
URN: urn:nbn:se:liu:diva-50407DOI: 10.1002/gcc.20222OAI: diva2:271303
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2010-05-24

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Department of Paediatrics in Linköping
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Genes, Chromosomes and Cancer
Natural Sciences

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