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Formation of a hyperdiploid karyotype in childhood acute lymphoblastic
leukemia [see comments]
N Onodera, NR McCabe and CM Rubin
Department of Pediatrics, University of Chicago, IL 60637.
Hyperdiploidy with greater than or equal to 50 chromosomes is a frequent
and distinct karyotypic pattern in the malignant cells of children with
acute lymphoblastic leukemia. To understand better the mechanism of
formation of the hyperdiploid karyotype, we studied 15 patients using 20
DNA probes that detect restriction fragment length polymorphisms. We first
examined disomic chromosomes for loss of heterozygosity. Two patients had
widespread loss of heterozygosity on all informative disomic chromosomes,
and represent cases of near- haploid leukemia in which the chromosomes
doubled. One other patient had loss of heterozygosity limited to chromosome
3; in this patient all of seven other informative disomic chromosomes
retained heterozygosity. Loss of heterozygosity was not detected in the
remaining 12 patients on a total of 87 informative disomic chromosomes. We
then examined tetrasomic chromosomes for parental dosage. Of the 13
patients in whom widespread loss of heterozygosity was not present, 11
patients had tetrasomy 21; 10 of 11 (91%) had an equal dose of maternal and
paternal alleles on chromosome 21 and only 1 of 11 (9%) had an unequal dose
of parental alleles in a 3:1 ratio. These results suggest that the
hyperdiploid karyotype usually arises by simultaneous gain of chromosomes
from a diploid karyotype during a single abnormal cell division, and
occasionally by doubling of chromosomes from a near- haploid karyotype. The
hyperdiploidy in cases without widespread loss of heterozygosity is not
caused by stepwise or sequential gains from a diploid karyotype or by
losses from a tetraploid karyotype; the former should result in a 3:1
parental dosage for 67% of tetrasomic chromosomes (9% observed) and the
latter should result in loss of heterozygosity for 33% of disomic
chromosomes (1% observed). Additional studies of the molecular basis for
this leukemia subtype are warranted.
Volume 80,
Issue 1,
pp. 203-208,
07/01/1992
Copyright © 1992 by The American Society of Hematology
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