|
|
Previous Article | Table of Contents | Next Article 
Interleukin-6 and granulocyte-macrophage colony-stimulating factor are
candidate growth factors for chronic myelomonocytic leukemia cells
MP Everson, CB Brown and MB Lilly
Department of Medicine, University of Alabama Birmingham.
Previous studies suggest that malignant cells from some patients with
myeloid leukemias produce colony-stimulating factors (CSFs) that can
function as autocrine growth factors in vitro. We have examined the roles
of interleukin-6 (IL-6) and granulocyte-macrophage CSF (GM-CSF) in the
proliferation of myeloid leukemia cells. IL-6 activity was assessed in
conditioned medium (CM) from myeloid leukemia cell cultures or cell lysates
using IL-6-dependent KD83 and 7TD1 murine cell lines. Media conditioned by
cells from patients with chronic myelomonocytic leukemia (CMMoL), but not
by normal monocytes, chronic myelogenous leukemia (CML), or acute
myelogenous leukemia (AML) cells, contained substantial levels (50 to 1,000
U/10(6) cells) of IL-6. The IL-6 content of CM correlated directly with
donor peripheral blood WBC count. CM from two of five CMMoL samples also
contained greater than 350 pg/mL GM-CSF. Moreover, CMMoL cells
spontaneously formed colonies in semisolid medium. CMMoL colony formation
could be partially inhibited by antibodies to IL-6 or GM-CSF, whereas
combination of these antibodies gave additive, and nearly complete (greater
than 93%), inhibition of spontaneous colony formation. Cell lysates from
uncultured CMMoL cells from one patient contained abundant GM-CSF protein
but no detectable IL-6. These data suggest that IL-6 and GM-CSF act in
vitro as autocrine growth factors for CMMoL cells, and that CMMoL cells in
vivo may represent a GM-CSF-dependent autocrine growth system.
Volume 74,
Issue 5,
pp. 1472-1476,
10/01/1989
Copyright © 1989 by The American Society of Hematology

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
A. F. List
New Approaches to the Treatment of Myelodysplasia
Oncologist,
April 1, 2002;
7(90001):
39 - 49.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. J. Arceci, B. J. Longley, and P. D. Emanuel
Atypical Cellular Disorders
Hematology,
January 1, 2002;
2002(1):
297 - 314.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
M. H. Tomasson, I. R. Williams, S. Li, J. Kutok, D. Cain, S. Gillessen, G. Dranoff, R. A. Van Etten, and D. G. Gilliland
Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3
Blood,
March 1, 2001;
97(5):
1435 - 1441.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. J. Guimaraes, J. F. Bazan, J. Castagnola, S. Diaz, N. G. Copeland, D. J. Gilbert, N. A. Jenkins, A. Varki, and A. Zlotnik
Molecular Cloning and Characterization of Lysosomal Sialic Acid O-Acetylesterase
J. Biol. Chem.,
June 7, 1996;
271(23):
13697 - 13705.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|
|