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Basophils (Bsp-1+) derive from the leukemic clone in human myeloid
leukemias involving the chromosome breakpoint 9q34
MP Bodger, CM Morris, MA Kennedy, JA Bowen, JM Hilton and PH Fitzgerald
Cytogenetic and Molecular Oncology Unit, Christchurch Hospital, New
Zealand.
The monoclonal antibody (MoAb) Bsp-1 was used to purify basophilic cells
from leukemic blood of five patients with Philadelphia chromosome (Ph')
positive chronic myeloid leukemia (CML) and two patients with acute myeloid
leukemia (AML) characterized by the chromosomal translocation
t(6;9)(p23;q34). When cultured, Bsp-1 positive cells from all CML and AML
patients showed the same clonal karyotype changes observed in diagnostic
buffy coat preparations, indicating that the basophilic cells were of
leukemic origin. In contrast, T lymphocytes from four of five CML patients
cultured in the presence of interleukin- 2 (IL-2) showed a normal karyotype
and were therefore not derived from the leukemic clone. Bsp-1 staining
correlated with toluidine blue- positive basophils in chronic phase CML and
with toluidine blue- negative blast cells expressing an immature myeloid
phenotype in blast crisis CML and AML. Chromosome in situ hybridization
showed that the ABL oncogene was translocated from chromosome 9 to
chromosome 22 in the CML patients but remained on chromosome 9 in the AML
patients. These results indicate that the breakpoint at 9q34 in CML is 5'
of ABL, whereas the breakpoint at 9q34 in AML is 3' of ABL. Field inversion
gel electrophoresis showed that the 9q34 breakpoint was not within 200 kb
3' of ABL in one of the AML patients, nor was there any rearrangement of
the PIM oncogene locus at 6p21.
Volume 73,
Issue 3,
pp. 777-781,
02/15/1989
Copyright © 1989 by The American Society of Hematology

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