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Differences in the frequency of normal and clonal precursors of colony-
forming cells in chronic myelogenous leukemia and acute myelogenous
leukemia
ID Bernstein, JW Singer, FO Smith, RG Andrews, DA Flowers, J Petersens, L Steinmann, V Najfeld, D Savage and S Fruchtman
Fred Hutchinson Cancer Research Center, Veterans Administration Medical
Center, Seattle, WA 98104.
Acute myelogenous leukemia (AML) is a clonal disease that is heterogeneous
with respect to the pattern of differentiative expression of the leukemic
progenitors. In some patients, the involved stem cells manifest pluripotent
differentiative expression, whereas in others, the involved progenitors
manifest differentiative expression mainly restricted to the granulocytic
pathway. This is in contrast to chronic myelogenous leukemia (CML) which is
a clonal disease known to arise in a pluripotent stem cell. Therefore, we
tested whether these leukemias could be distinguished with respect to their
involvement of immature precursors by studying colony-forming cells (CFC)
and their precursors from four glucose-6-phosphate dehydrogenase (G6PD)
heterozygous patients with AML and five patients with CML. CFC were
separated from their precursors by FACS for expression of CD33 and CD34
followed by growth in a long-term culture (LTC) system. The vast majority
of CFC express both the CD33 and CD34 antigens, but their less mature
precursors, detected by their ability to give rise to CFC in LTC, express
only CD34. In three of the four patients with AML, the CD33- CD34+ cells
produced CFC in LTC that appeared to be predominantly or completely normal
(ie, nonclonal) in origin. In the fourth patient, a significant enrichment
of nonclonal progenitors was obtained in the CD33-CD34+ population, but
these cells may also have included significant numbers of clonal cells. In
contrast, in four of five patients with CML, cultures of both the
CD33-CD34+ and CD33+CD34+ populations produced CFC in LTC that were almost
entirely clonal in origin, whereas in the fifth patient a substantial
number originated from nonclonal stem cells. These data indicate that
granulocyte/monocyte progenitors are predominantly clonally derived in CML
and AML. In CML, their precursors are also predominantly clonal, but in
some cases of AML they are not. These findings may have implications for
understanding the success or failure of current therapies of AML and CML.
Volume 79,
Issue 7,
pp. 1811-1816,
04/01/1992
Copyright © 1992 by The American Society of Hematology
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