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Chromosomal loss and deletion are the most common mechanisms for loss of
heterozygosity from chromosomes 5 and 7 in malignant myeloid disorders
WL Neuman, CM Rubin, RB Rios, RA Larson, MM Le Beau, JD Rowley, JW Vardiman, JL Schwartz and RA Farber
Department of Medicine, University of Chicago, IL.
We have examined a population of patients with acute myeloid leukemia (AML)
or myelodysplastic syndrome (MDS) for loss of heterozygosity of polymorphic
markers on chromosomes 5 and 7. The rationale for this study was the
observation that the majority of patients with therapy- related leukemia
(t-AML or t-MDS), resulting from cytotoxic treatment for prior
malignancies, have loss of chromosome 5 and/or 7 or deletions involving the
long arms of one or both of these chromosomes. This cytogenetic finding
suggested that tumor-suppressor genes, important in the development of AML,
may be located in these chromosomal regions. We analyzed a total of 60
patients, 43 with primary MDS/AML de novo and 17 with t-MDS/t-AML. Leukemia
cells were evaluated for restriction fragment length polymorphisms (RFLPs).
Leukemia cell genotypes were compared with lymphoblastoid cell genotypes
from the same patients. Two cases of loss of heterozygosity were identified
from chromosomes lacking visible deletions: one involving chromosome 5 in a
patient with AML de novo who had a visible deletion of 5q at a later stage
of the disease, and one involving chromosome 7 in a patient with t-AML. We
conclude that allele loss from loci on chromosomes 5 and 7 in MDS/AML, when
it occurs, usually results from major deletion or simple chromosome loss,
rather than from mitotic recombination or chromosome loss with duplication
of the remaining homologue.
Volume 79,
Issue 6,
pp. 1501-1510,
03/15/1992
Copyright © 1992 by The American Society of Hematology
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