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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2338-2344
MCP-1, not MIP-1 , Is the Endogenous Chemokine That Cooperates
With TGF- to Inhibit the Cycling of Primitive Normal but not
Leukemic (CML) Progenitors in Long-Term Human Marrow Cultures
J.D. Cashman,
C.J. Eaves,
A.H. Sarris, and
A.C. Eaves
From the Terry Fox Laboratory, British Columbia Cancer Agency and the
Departments of Medical Genetics, Medicine, and Pathology, University of
British Columbia, Vancouver, BC, Canada; and the Department of
Lymphoma/Myeloma, University of Texas, MD Anderson Cancer Center,
Houston, TX.
The long-term culture (LTC) system has been useful for
analyzing mechanisms by which stromal cells regulate the proliferative activity of primitive normal, but not chronic myeloid leukemia (CML),
hematopoietic progenitor cells. In previous studies, we identified two
endogenous inhibitors in this system. One is transforming growth
factor- (TGF-), which is equally active on primitive normal and
CML progenitors. The other we now show to be monocyte chemoattractant
protein-1 (MCP-1). Thus, MCP-1, when added to LTC, blocked the
activation of primitive normal progenitors but did not arrest the
cycling of primitive CML progenitors. Moreover, the endogenous
inhibitory activity of LTC stromal layers could be overcome by the
addition of neutralizing antibodies to MCP-1, but not to macrophage
inflammatory protein-1 (MIP-1). However, neither of these
antibodies antagonized the inhibitory activity of NAc-Ser-Asp-Lys-Pro
(AcSDKP) on primitive normal but not CML progenitor cycling in this
system. Moreover, none of six other -C-C- or -C-X-C- chemokines,
previously shown to inhibit primitive normal human CFC proliferation in
semisolid assays, were found to act as negative regulators when added
to normal LTC. These results provide further support for the concept
that primitive CML progenitor cell proliferation is deregulated when
these cells are exposed to limiting concentrations of multiple
inhibitors, only some of which have differential actions on normal and
Ph+/BCR-ABL+ cells.
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