Document Detail

Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia.
MedLine Citation:
PMID:  15942938     Owner:  NLM     Status:  MEDLINE    
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.
Kajsa Paulsson; Helena Mörse; Thoas Fioretos; Mikael Behrendtz; Bodil Strömbeck; Bertil Johansson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Genes, chromosomes & cancer     Volume:  44     ISSN:  1045-2257     ISO Abbreviation:  Genes Chromosomes Cancer     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-08-08     Completed Date:  2005-09-26     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9007329     Medline TA:  Genes Chromosomes Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  113-22     Citation Subset:  IM    
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden.
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MeSH Terms
Cell Division
Genetic Markers
In Situ Hybridization, Fluorescence
Microsatellite Repeats / genetics
Polymerase Chain Reaction
Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*,  pathology
Reg. No./Substance:
0/Genetic Markers

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