Effects of recombinant human GM-CSF on proliferation of clonogenic cells in acute myeloblastic leukemia

Griffin, James D.; Dc, Young; Herrmann, F; Wiper, Donald W.; Wagner, Katherine; Sabbath, Kert D.

doi:10.1182/blood.v67.5.1448.1448

Cited by 208 publications

(13 citation statements)

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“…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). Furthermore, the proliferation of some AML cells has been supported by rhGM-CSF (Griffin et al, 1986;Hoang et al, 1986). The establishment of three GM-CSF-dependent cell lines (T-ALL-101, AML 193, and MV4-11) has been reported recently (Lange et al, 1987;Valtieri et al, 1987).…”

Section: Induction Of Differentiation By Various Agentsmentioning

confidence: 96%

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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Section: Induction Of Differentiation By Various Agentsmentioning

confidence: 96%

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

View full text Add to dashboard Cite

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“…Despite their high proliferative rate in vivo, most leukemic cells do not grow well in tissue culture (Ferrero and Rovera, 1984). However, since the identification and purification of hemopoietic growth factors such as IL-3, GM-CSF, G-CSF, M-CSF, or cytokines such as IL-1 and IL-6, the short-term proliferation in vitro of AML cells isolated from patients has been more readily achieved (Griffin et al, 1986;Miyauchi et al, 1987). Most AML cells proliferate in the presence of G-CSF, GM-CSF, IL-3 (Santoli et al, 1987), or IL-I (Cozzolino et al, 1989;Delwel et al, 1989).…”

mentioning

confidence: 99%

Growth regulation of the AML‐193 leukemic cell line: Evidence for autocrine production of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and inhibition of GM‐CSF‐dependent cell proliferation by interleukin‐1 (IL‐1) and tumor necrosis factor (tnfα)

Kindler¹,

Shields²,

Ayer³

et al. 1991

Intl Journal of Cancer

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The human leukemic cell line AML-193 was tested for its proliferative response to endogenously produced autocrine factors and to a variety of cytokines and colony-stimulating factors. Cells grown in the absence of GM-CSF incorporated tritiated thymidine, and this was partially reversed by adding neutralizing anti-GM-CSF antibodies to the culture medium, suggesting that it was due, at least in part, to autocrine GM-CSF production. This was confirmed by immunopurification of a GM-CSF-like activity from cell supernatant of AML-193 cells grown in serum free medium in the absence of exogenous GM-CSF. When AML-193 cells were cultured with GM-CSF in combination with other cytokines, Interleukin-1 alpha and beta (IL-1 alpha and beta), Interleukin-3 (IL-3), Interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and tumor necrosis factor alpha (TNF alpha), none of them affected the concentration of GM-CSF required to induce 50% of maximum proliferation (D50). However, the maximum proliferation induced by GM-CSF alone was drastically decreased by IL-1 alpha, IL-1 beta and TNF alpha. Inhibition caused by exposure of the AML-193 to IL-1 for up to 24 hr was reversible, ruling out a direct cytotoxic effect.

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“…Highly purified or recombinant CSF is a candidate for studying the regulation of the proliferation of the leukemic blast progenitors. Recently, the effects of recombinant GM-CSF on leukemic blast progenitors have been studied; recombinant GM-CSF supported the self-renewal and terminal divisions of blast progenitors from AML patients [10,11]. The data have demonstrated that a factor regulating normal granulopoiesis also stimulates the growth of the leukemic population.…”

Section: Introductionmentioning

confidence: 99%

Effects of purified human native granulocyte colony‐stimulating factor (G‐CSF) on proliferation of blast progenitors in acute myeloblastic leukemia

et al. 1988

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Blast progenitors in acute myeloblastic leukemia (AML) grow in methylcellulose and suspension cultures. Blast colony formation in methylcellulose culture reflects the terminal divisions of blast progenitors, while secondary colony formation, by replating in methylcellulose and recovering clonogenic cells in suspension culture, reflects the self-renewal of blast progenitors. To analyze the regulatory mechanisms of the proliferation of leukemic blast progenitors, the effects of highly purified native granulocyte colony-stimulating factor (G-CSF) obtained from human squamous cell carcinoma line (CHU-2) on blast progenitors in AML patients were studied in methylcellulose and suspension cultures. Purified G-CSF stimulated the growth of blast progenitors in both culture systems, although sensitivity to G-CSF varied from patient to patient. No obvious maturation of leukemic blasts was noted in suspension culture in the presence of G-CSF. The data suggest that a normal hemopoietic regulator may play a role in the growth of blast progenitors in AML patients.

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Effects of recombinant human GM-CSF on proliferation of clonogenic cells in acute myeloblastic leukemia

Cited by 208 publications

References 0 publications

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

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

Growth regulation of the AML‐193 leukemic cell line: Evidence for autocrine production of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and inhibition of GM‐CSF‐dependent cell proliferation by interleukin‐1 (IL‐1) and tumor necrosis factor (tnfα)

Effects of purified human native granulocyte colony‐stimulating factor (G‐CSF) on proliferation of blast progenitors in acute myeloblastic leukemia

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