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Blood, Vol. 92 No. 11 (December 1), 1998:
pp. 4031-4035
RAPID COMMUNICATION
Molecular Cytogenetic Characterization of a Critical Region in Bands
7q35-q36 Commonly Deleted in Malignant Myeloid Disorders
Konstanze Döhner,
Jill Brown,
Ute Hehmann,
Claudia Hetzel,
Janet Stewart,
Gordon Lowther,
Claudia Scholl,
Stefan Fröhling,
Antonio Cuneo,
Lap C. Tsui,
Peter Lichter,
Stephen W. Scherer, and
Hartmut Döhner
From Medizinische Klinik and Poliklinik V, University of Heidelberg,
Heidelberg, Germany; Duncan Guthrie Institute of Medical Genetics,
Glasgow, UK; Dipartimento di Scienze Biomediche e Terapie Avanzate
Universita Degli Studi di Ferrara, Ferrara, Italy; the
Department of Genetics, The Hospital for Sick Children, Toronto,
Ontario, Canada; and Abteilung "Organisation komplexer Genome,"
Deutsches Krebsforschungszentrum, Heidelberg, Germany.
Loss of chromosome 7 ( 7) or deletion of the long arm (7q) are
recurring chromosome abnormalities in myeloid leukemias. The association of 7/7q with myeloid leukemia suggests that these regions contain novel tumor suppressor gene(s), whose loss of function
contribute to leukemic transformation or tumor progression. Based on
chromosome banding analysis, two critical regions have been identified,
one in band q22 and another in bands q32-q35. Presently there are no
data available on the molecular delineation of the distal critical
region. In this study we analyzed bone marrow and blood samples from 13 patients with myeloid leukemia (de novo myelodysplastic syndrome
[MDS] , n = 3; de novo acute myeloid leukemia [AML], n = 9;
therapy-related (t-) AML, n = 1) which, on chromosome banding
analysis, exhibited deletions (n = 12) or in one case a balanced
translocation involving bands 7q31-qter using fluorescence in situ
hybridization (FISH). As probes we used representative clones from a
contig map of yeast artificial chromosome (YAC) clones that spans
chromosome bands 7q31.1-qter. In the 12 cases with loss of 7q material,
we identified a commonly deleted region of approximately 4 to 5 megabasepairs in size encompassing the distal part of 7q35 and the
proximal part of 7q36. Furthermore, the breakpoint of the reciprocal
translocation from the patient with t-AML was localized to a 1,300-kb
sized YAC clone that maps to the proximal boundary of the commonly
deleted region. Interestingly, in this case both homologs of chromosome 7 were affected: one was lost (7) and the second exhibited the t(7q35). The identification and delineation of translocation and deletion breakpoints provides the first step toward the identification of the gene(s) involved in the pathogenesis of 7q35-q36 aberrations in
myeloid disorders.
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