Growth factor-mediated tumor cell proliferation in hairy cell leukemia.

Ford, R.; Yoshimura, Linda C.; Morgan, John; Quesada, Jorge R.; Montagna, Richard A.; Maizel, Abby

doi:10.1084/jem.162.3.1093

Cited by 45 publications

(5 citation statements)

References 13 publications

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“…It is more difficult to assess the relative importance of each cytokine downregulated by IFN-a treatment . TNF (8, 12, 24), IIr1(5), BCGF (25)(26)(27), and IIr6 (28) may all be capable of inducing growth and/or differentiation in B-CLL/HCL cells, so that the overall therapeutic effects of IFN-a may result from the downregulation of a multiplicity of endogenous growth factors .…”

Section: Methodsmentioning

confidence: 99%

Effects of interferon alpha on autocrine growth factor loops in B lymphoproliferative disorders.

Heslop

Bianchi

Cordingley

et al. 1990

The Journal of Experimental Medicine

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The B lymphoproliferative disorders B chronic lymphocytic leukemia (B-CLL) and hairy cell leukemia (HCL) produce a number of autocrine growth factors, including tumor necrosis factor (TNF), interleukin 6 (IL-6), and IL-1, all of which may induce positive feedback growth loops. If such malignancies depend on these autocrine growth loops for survival, their interruption may be therapeutically valuable. Interferon alpha (IFN-alpha) abrogates TNF- or IL-6-induced proliferation of HCL and B-CLL cells in vitro and has therapeutic activity in these diseases. We have investigated the possibility that IFN-alpha may act by interrupting autocrine growth factor loops. If purified B-CLL or HCL cells are cultured in the presence of TNF, there is induction of mRNA for TNF, IL-1 alpha, IL-1 beta, and IL-6. However, culture in the presence of IFN-alpha in addition to TNF reduced the level of mRNA for all these cytokines, compared with cells cultured in TNF alone. While cytokine mRNA levels were diminished, levels of mRNA for the ribonuclease activator 2-5A synthetase were increased. Analysis of the kinetics of cytokine mRNA production showed that levels fall shortly after the rise of 2-5A synthetase mRNA. IFN-alpha may produce these effects by shortening the half-life of cytokine mRNA, since TNF mRNA half-life in B-CLL and HCL cells is substantially reduced when the cells are cultured with IFN-alpha. These data suggest that IFN-alpha may mediate its therapeutic effects in these malignancies by blocking autocrine growth factor loops.

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Section: Methodsmentioning

confidence: 99%

Effects of interferon alpha on autocrine growth factor loops in B lymphoproliferative disorders.

Heslop

Bianchi

Cordingley

et al. 1990

The Journal of Experimental Medicine

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“…Human IL-2 is well known to support the in vitro growth of differentiated T-cell leukemia cells such as Sezary T-cell leukemic cells (Poiesz et al, 1980) or adult T-cell leukemic cells (Hoshino et al, 1983). Similarly, human B-cell growth factor stimulates the growth of hairy cell leukemic cells (Ford et al, 1985). Some acute myelogenous leukemia (AML) cells have the ability to form colonies in a semisolid culture supplemented with conditioned media containing colonystimulation factors (Moore et al,, 1973;Griffin and Lo- , 1986).…”

Section: Induction Of Differentiation By Various Agentsmentioning

confidence: 99%

Establishment and characterization of a unique human cell line that proliferates dependently on GM‐CSF, IL‐3, or erythropoietin

Kitamura¹,

Tange²,

Terasawa³

et al. 1989

Journal Cellular Physiology

789

459

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We have established a novel cell line, designated as TF-1, from a patient with erythroleukemia, which showed complete growth dependency on granulocyte-macrophage colony-stimulating factor (GM-CSF) or on interleukin-3 (IL-3) and carried a homogeneous chromosomal abnormality (54X). Erythropoietin (EPO) also sustained the short-term growth of TF-1, but did not induce erythroid differentiation. These three hematopoietic growth factors acted on TF-1 synergistically. Transforming growth factor-beta and interferons inhibited the factor-dependent growth of TF-1 cells in a dose-dependent fashion, and monocyte-colony stimulating factor and interkeukin-1 enhanced the GM-CSF-dependent growth of TF-1. Ultrastructural studies revealed some very immature features in this cell line. Although TF-1 cells do not express glycophorin A or carbonyl anhydrase I, the morphological and cytochemical features, and the constitutive expression of globin genes, indicate the commitment of TF-1 to erythroid lineage. When induced to differentiate, TF-1 entered two different pathways. Specifically, hemin and delta-aminolevulinic acid induced hemoglobin synthesis, whereas TPA induced dramatic differentiation of TF-1 into macrophage-like cells. In summary, TF-1 is a cell line of immature erythroid origin that requires GM-CSF, IL-3, or EPO for its growth and that has the ability to undergo differentiation into either more mature erythroid cells or into macrophage-like cells. TF-1 is a useful tool for analyzing the human receptors for IL-3, GM-CSF, and EPO or the signal transduction of these hemopoietic growth factors.

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“…4,5 They display clonal surface immunoglobulins and express the CD19, CD20, CD22, CD79a, CD25 and CD103 markers, 6 less frequently CD38, CD45RO, CD23, CD15, CD4, CD5 and CD10. 7,8 Proliferation of the HCL tumoral cells is regulated by growth factors 9,10 including cytokines and cytokine antagonists and there is a correlation between circulating soluble interleukin-2 receptor (sIL-2R) levels and disease activity. Our group showed previously that the remission achieved by IFN-␣ treatment was correlated with a marked reduction in the serum level of soluble CD23 or sCD23 11 in agreement with the proposed role of CD23 and its soluble cleavage fragment in the proliferation and anti-apoptotic effect in chronic B cell malignancies.…”

Section: Introductionmentioning

confidence: 99%

Expression of a functional inducible nitric oxide synthase in hairy cell leukaemia and ESKOL cell line

et al. 2000

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Growth factor-mediated tumor cell proliferation in hairy cell leukemia.

Cited by 45 publications

References 13 publications

Effects of interferon alpha on autocrine growth factor loops in B lymphoproliferative disorders.

Effects of interferon alpha on autocrine growth factor loops in B lymphoproliferative disorders.

Establishment and characterization of a unique human cell line that proliferates dependently on GM‐CSF, IL‐3, or erythropoietin

Expression of a functional inducible nitric oxide synthase in hairy cell leukaemia and ESKOL cell line

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