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Evidence that stem cell factor is involved in the rebound thrombocytosis
that follows 5-fluorouracil treatment
P Hunt, KM Zsebo, MM Hokom, A Hornkohl, NC Birkett, JC del Castillo and F Martin
Amgen, Laboratory of Stem Cell Biology, Amgen Center, Thousand Oaks, CA
91320.
The mechanisms responsible for 5-fluorouracil (5FU)-induced rebound
thrombocytosis are not completely understood. SI/SI(d) mice, which do not
undergo rebound thrombocytosis in response to 5FU, provide a genetic
approach to the study of this phenomenon. Recent reports by several groups
that the SI locus encodes a protein known variably as stem cell factor
(SCF), mast cell growth factor, or kit ligand, suggests the possibility
that the lack of wild-type SCF in SI/SI(d) mice is responsible for their
defective response to 5FU-induced thrombocytopenia. It is shown in this
report that SCF-treated SI/SI(d) mice are as capable as their wild-type
littermates in undergoing rebound thrombocytosis. W/Wv mice, mutated at the
locus encoding the SCF receptor, also do not undergo rebound
thrombocytosis, but are not responsive to SCF treatment. In normal mice, it
is shown by RNA solution hybridization that SCF mRNA expression is
increased during the 5FU-induced platelet nadir period. It is also shown by
autoradiography that maturing megakaryocytes express SCF receptors, and
that in vivo administration of SCF significantly raises the numbers of
megakaryocytes, as well as circulating platelet counts. Taken together,
these data indicate that SCF may be an important regulator of platelet
production under both normal and physiologically disturbed situations.
Volume 80,
Issue 4,
pp. 904-911,
08/15/1992
Copyright © 1992 by The American Society of Hematology
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