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Clonal analysis of bcr-abl rearrangement in T lymphocytes from patients
with chronic myelogenous leukemia
D Jonas, M Lubbert, ES Kawasaki, M Henke, KJ Bross, R Mertelsmann and F Herrmann
Department of Hematology/Oncology, University of Freiburg Medical Center,
Germany.
The cytogenetic hallmark of chronic myelogenous leukemia (CML) is the
Philadelphia chromosome (Ph1), which reflects a chromosomal translocation
t(9;22) and a rearrangement of the ABL and bcr genes. This marker is found
in all cells arising from the same malignant precursor cell and can be
detected in CML cells of the myeloid, monocytic, erythroid, and
B-lymphocyte lineage. It is, however, controversial as to whether T
lymphocytes of CML patients carry this gene rearrangement. An answer to
this question would clarify whether the translocation in CML occurs in a
pluripotent hematopoietic stem cell or in a precursor cell already
committed to certain lineages, but not the T-cell lineage. To address this
question, we established T-cell clones from peripheral venous blood cells
of four patients with CML and screened these clones for bcr-abl fusion
transcripts by means of polymerase chain reaction and Southern blot
analysis. In four T-cell clones of three of these patients, the bcr-abl
transcript could be detected. None of 12 T-cell clones of the fourth
patient disclosed detectable bcr-abl amplification product. Both CD4+ as
well as CD8+ clones displayed fused bcr-abl sequences. These data imply
that in CML some but not all T lymphocytes may originate from the
Ph1-positive stem cell.
Volume 79,
Issue 4,
pp. 1017-1023,
02/15/1992
Copyright © 1992 by The American Society of Hematology
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