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Molecular analysis of chromosome 20q deletions associated with
myeloproliferative disorders and myelodysplastic syndromes
FA Asimakopoulos, NJ White, E Nacheva and AR Green
Department of Haematology, University of Cambridge, MRC Centre, UK.
Acquired deletions of the long arm of chromosome 20 are found in several
hematologic conditions and particularly in the myeloproliferative disorders
and myelodysplastic syndromes. The spectrum of diseases associated with 20q
deletions suggests that such deletions may mark the site of a tumor
suppressor gene that contributes to the regulation of normal multipotent
hematopoietic progenitors. We present here the first detailed molecular
analysis of 20q deletions associated with myeloid disorders. Thirty-four
microsatellite primer pairs corresponding to loci on 20q have been used to
study DNA samples from two cell lines and from highly purified peripheral
blood granulocytes obtained from seven patients. In addition, Southern
analysis of cell line DNA has been performed using 19 DNA probes that map
to 20q. Three conclusions can be drawn from our results. Firstly, molecular
heterogeneity of both centromeric and telomeric breakpoints was
demonstrated, thus supporting the existence of a tumor suppressor gene on
20q. In addition many of the breakpoints have been mapped to small genetic
intervals. Secondly, our results define a commonly deleted region of 16-21
cM which contains ADA, PLC1, TOP1, SEMG1, and PPGB. Several candidate tumor
suppressor genes lie outside the common deleted region including SRC, HCK,
p107, PTPN1, and CEBP beta. Thirdly, the data allow integration of genetic
and physical maps and have refined the map positions of multiple genes.
These results will facilitate attempts to identify candidate hematopoietic
tumor suppressor genes on 20q.
Volume 84,
Issue 9,
pp. 3086-3094,
11/01/1994
Copyright © 1994 by The American Society of Hematology
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