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Variable transcription of BCR-ABL by Ph+ cells arising from hematopoietic
progenitors in chronic myeloid leukemia [see comments]
A Keating, XH Wang and P Laraya
Toronto Hospital, Ontario, Canada.
Recent studies suggest that the BCR-ABL gene plays a critical role in the
pathogenesis of Ph+ chronic myeloid leukemia (CML). We investigated the
hematopoietic colonies derived from the marrows of 12 patients with Ph+ CML
in chronic phase by reverse transcriptase-polymerase chain reaction
(RT-PCR) amplification of BCR-ABL mRNA and by cytogenetics. Colonies were
individually harvested and each colony divided into two portions, one for
cytogenetics and the other for isolation of total RNA for PCR of BCR-ABL
transcripts and for an RNA internal control. We found that 23% +/- 18%
(mean +/- SD, range 0% to 60%) of Ph+ colonies did not transcribe the
aberrant gene. In each case when BCR-ABL transcription was not detected,
normal ABL mRNA was present. The data suggest that hitherto unknown
mechanisms may regulate BCR-ABL expression in some Ph+ cells and indicate
that caution should be exercised in the interpretation of results using
RT-PCR analysis of hematopoietic colonies from clinical specimens and from
experiments with antisense oligonucleotides directed at the BCR-ABL gene.
These data also raise the notion of a transitional Ph+ precursor cell in
which BCR-ABL may become upregulated and lead to a fully expressed
phenotype. We conclude that further studies correlating the frequency of
Ph+ PCR- progenitors with prognostic clinical variables are warranted.
Volume 83,
Issue 7,
pp. 1744-1749,
04/01/1994
Copyright © 1994 by The American Society of Hematology
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