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bcr rearrangement and translocation of the c-abl oncogene in Philadelphia
positive acute lymphoblastic leukemia
A De Klein, A Hagemeijer, CR Bartram, R Houwen, L Hoefsloot, F Carbonell, L Chan, M Barnett, M Greaves and E Kleihauer
The Philadelphia (Ph1) chromosome, the cytogenetic hallmark of chronic
myeloid leukemia (CML), has also been detected in a significant number of
acute lymphoblastic leukemias (ALL). Using in situ hybridization, we
demonstrate that in accordance with observations in CML the Ph1 chromosome
in ALL patients is the result of a consistent translocation of the c-abl
oncogene to the Ph1 chromosome. Southern blot analysis using bcr probes,
however, suggests that Ph1-positive ALL includes heterogeneous leukemic
subtypes: six ALL patients showed bcr rearrangements as observed in CML; in
three other patients recombination involving 5' bcr sequences could be
demonstrated, but the corresponding translocated 3' bcr sequences were not
detectable. A third group of five patients did not show any bcr
rearrangements at all. Northern blot analysis using RNA from three
Ph1-positive ALL patients revealed that in the leukemic cells of two
patients larger c- abl mRNA transcripts were present, as in CML. In the RNA
of one patient without a detectable bcr rearrangement, only the normal
c-abl mRNA transcripts are present. The observed heterogeneity in bcr
rearrangements of this group of Ph1-positive ALL patients is in contrast
with the consistent results obtained in more than 50 Ph1- positive CML
patients investigated in chronic and acute states.
Volume 68,
Issue 6,
pp. 1369-1375,
12/01/1986
Copyright © 1986 by The American Society of Hematology
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