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Chromosome 7 long arm deletion in myeloid disorders: a narrow breakpoint
region in 7q22 defined by molecular mapping
J Kere, T Ruutu, KA Davies, IB Roninson, PC Watkins, R Winqvist and A de la Chapelle
Department of Medical Genetics, University of Helsinki, Finland.
The involvement of the erythropoietin (EPO), plasminogen activator
inhibitor type I (PAI1), and multi-drug resistance (MDR2) genes located in
chromosomal region 7q21-22 was studied in patients with myeloid disorders
and with or without a chromosome 7 abnormality. Separated blood mononuclear
cells and granulocytes from 21 patients were used in restriction fragment
length polymorphism (RFLP) studies with gene- specific DNA probes. A marked
weakness of one of the allelic bands was observed in granulocyte-derived
DNA from heterozygous patients with monosomy 7. In four patients with a
partial deletion of chromosome 7 long arm (7q-), marked weakness of an
allelic band was observed in granulocyte-derived DNA with PAI1 probe (four
heterozygous patients) and MDR2 probe (one heterozygous patient), implying
deletion of these genes. In contrast, the EPO gene was not deleted in these
patients, as demonstrated by the presence of two allelic bands of equal
strength in granulocyte-derived DNA (two patients) or by gene dosage
estimation (two patients). Two allelic bands of equal strength were also
observed in three heterozygous patients with an arbitrary probe (pKV13)
located in 7cen-q21.3. Unexpected hemizygosity or hybridization bands were
not observed in any patient. We conclude that PAI1 and MDR2 are located
distally of EPO in 7q22, and that none of these genes is commonly
rearranged in myeloid disorders. The chromosome 7 long arm deletion
breakpoint is located in a relatively narrow segment between the PAI1 and
EPO genes in different patients. The deletion may involve a specific site
in DNA, since the genetic distance between the PAI1 and EPO genes is only 3
cM.
Volume 73,
Issue 1,
pp. 230-234,
01/01/1989
Copyright © 1989 by The American Society of Hematology
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