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Blood, Vol. 95 No. 6 (March 15), 2000:
pp. 1883-1890
PLENARY PAPER
Prognostic implications of differences in telomere length
between normal and malignant cells from patients with chronic
myeloid leukemia measured by flow cytometry
Tim H. Brümmendorf,
Tessa L. Holyoake,
Nathalie Rufer,
Michael J. Barnett,
Michael Schulzer,
Connie J. Eaves,
Allen C. Eaves, and
Peter M. Lansdorp
From the Terry Fox Laboratory and Division of Hematology, British
Columbia Cancer Agency, Vancouver, British Columbia, Canada;
Departments of Medicine, Statistics, and Medical Genetics, University
of British Columbia, Vancouver, British Columbia, Canada.
Chronic myeloid leukemia (CML) is a clonal, multilineage
myeloproliferative disorder characterized by the Philadelphia
chromosome (Ph) and a marked expansion of myeloid cells. Previous
studies have indicated that the telomere length in blood cells may
indicate their replicative history. However, the large variation in
telomere length between individuals complicates the use of this
parameter in CML and other hematologic disorders. To circumvent this
problem, we compared the telomere length in peripheral blood or bone
marrow cells with purified normal (Ph ) T lymphocytes
from the same CML patient using fluorescence in situ hybridization and
flow cytometry. Overall telomere fluorescence was significantly reduced
in Ph+ cells from patients with CML compared to blood
leukocytes from normal individuals (P < 0.001) or normal
(Ph) T lymphocytes from the same individuals
(n = 51, P < 0.001). Cells from patients in accelerated
phase or blast phase (AP/BP) showed significantly shorter average
telomere length than cells from patients in chronic phase (CP,
P = 0.02) or cytogenetic remission (CR,
P = 0.03). Patients in CP who subsequently developed BP
within 2 years had significantly shorter telomeres than those who did not develop BP for at least 2 years (P < 0.05). Accelerated
replication-dependent telomere shortening in Ph+ versus
Ph leukocytes supports previous evidence that
Ph+ stem cells cycle more actively than their
counterparts in normal individuals. Our data further suggest that
telomere shortening may serve as a surrogate marker of disease
progression in patients with CP CML, supporting a mechanistic link
between CML stem cell turnover, genetic instability, and malignant
evolution in this disease. (Blood.
2000;95:1883-1890)
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