Induction of Differentiation in Myeloid Leukemic Cells and the Differentiation Inducing Factor (DIF)

1987 ◽  
pp. 51-59
Author(s):  
U. Gullberg ◽  
I. Olsson
Keyword(s):  
Leukemic Cells ◽  
Induction Of Differentiation

Induction of differentiation of cultured mouse myeloid leukemic cells by arginase

1979 ◽  
Vol 89 (3) ◽  
pp. 879-884 ◽  
Author(s):  
Junko Okabe ◽  
Moriaki Hayashi ◽  
Yoshio Honma ◽  
Motoo Hozumi
Keyword(s):  
Leukemic Cells ◽  
Induction Of Differentiation

scholarly journals Induction of differentiation of WEHI-3B D+ leukemic cells transfected with differentiation-stimulating factor/leukemia inhibitory factor receptor cDNA

Blood ◽  
1995 ◽  
Vol 85 (1) ◽  
pp. 217-221 ◽  
Author(s):  
M Tomida
Keyword(s):  
Leukemia Inhibitory Factor ◽  
Oncostatin M ◽  
Inhibitory Factor ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Leukemia Inhibitory Factor Receptor ◽  
Transfected Cells ◽  
Receptor Cdna ◽  
Induction Of Differentiation ◽  
Stimulating Factor

Differentiation-stimulating factor (D-factor)/leukemia inhibitory factor can induce the differentiation of mouse myeloid leukemia M1 cells and also stimulate proliferation of the interleukin-3 (IL-3)- dependent cell line, DA-1a. To determine whether D-factor can induce the differentiation of leukemia cells other than M1 cells, WEHI-3B D+ mouse myelomonocytic leukemia cells were transfected with a plasmid containing mouse D-factor receptor cDNA. Expression of D-factor receptor in transfected cells was determined by binding of [125]D- factor and analyzed by Scatchard's method. The transfected cells had high-affinity D-factor receptors with a dissociation constant of 100 to 200 pmol/L and binding sites per cell varied from 67 to 1,500 among several clones. The cells expressing a high level of D-factor receptor were induced to differentiate by D-factor; about 60% of the cells exhibited the ability to reduce nitroblue tetrazolium and expression of the differentiation antigen Mac-1 (CD11b) on the cell surface increased. The effect of cytokines, which induce the differentiation of M1 cells, on the transfected WEHI-3B cells was examined. The sensitivity to oncostatin M was identical to that against D-factor in the cells of each clone. Expression of D-factor receptor in WEHI-3B cells promoted sensitivity to IL-6 and granulocyte colony-stimulating factor (G-CSF). Induction of differentiation of the cells accompanied the suppression of proliferation. Treatment of the cells with D-factor for longer than 5 days resulted in 50% inhibition of growth. These results indicate that the stimulating effect of D-factor on the differentiation of malignant myeloid cells is not unique to M1 cells.

scholarly journals Inhibition of differentiation and affinity purification with a monoclonal antibody to a myeloid cell differentiation-inducing protein

Blood ◽  
1988 ◽  
Vol 72 (5) ◽  
pp. 1543-1549 ◽  
Author(s):  
Y Shabo ◽  
L Sachs
Keyword(s):  
Monoclonal Antibody ◽  
Affinity Purification ◽  
Myeloid Cell ◽  
Leukemic Cells ◽  
Endogenous Production ◽  
Mouse Macrophages ◽  
Induction Of Differentiation ◽  
Inhibition Of Differentiation ◽  
Necrosis Factor

Abstract The normal myeloid hematopoietic regulatory proteins include four growth-inducing proteins called colony-stimulating factors (CSF), including interleukin-3 (IL-3), or macrophage and granulocyte inducers, type 1 (MGI-1), and another type of protein (MGI-2) with no myeloid cell growth-inducing activity that induces differentiation of normal myeloid precursor cells and certain clones of myeloid leukemic cells. An IgG2a monoclonal antibody was prepared and it neutralized two forms of MGI-2 (MGI-2A and MGI-2B) produced by mouse Krebs ascites tumor cells. The monoclonal antibody was used for affinity purification of MGI-2. This antibody also neutralized MGI-2 produced by normal mouse macrophages, normal myeloblasts incubated with IL-3, and MGI-2 produced by the lungs and found in the serum of mice injected with lipopolysaccharide (LPS). The anti-MGI-2 antibody did not inhibit the activity of any one of the four myeloid growth-inducing proteins (CSF or IL-3 = MGI-1), IL-1, tumor necrosis factor, or lymphotoxin. This antibody also inhibited induction of differentiation of myeloid leukemic cells by LPS, which is mediated by the endogenous production of MGI-2, but did not inhibit induction of differentiation in these leukemic cells by dexamethasone or cytosine arabinoside, which is not mediated by MGI-2. Anti-MGI-2 antibody thus inhibited differentiation when MGI-2 was added externally to cells or when it was mediated by endogenously produced MGI-2.

scholarly journals Regulation of acid phosphatase activity in human promyelocytic leukemic cells induced to differentiate in culture.

1979 ◽  
Vol 83 (2) ◽  
pp. 300-307 ◽  
Author(s):  
A Vorbrodt ◽  
P Meo ◽  
G Rovera
Keyword(s):  
Endoplasmic Reticulum ◽  
Acid Phosphatase ◽  
Smooth Endoplasmic Reticulum ◽  
Leukemic Cell ◽  
Time Sequence ◽  
Leukemic Cells ◽  
Leukemic Cell Line ◽  
Faint Band ◽  
Induction Of Differentiation ◽  
Sequence Study

Induction of differentiation of a human promyelocytic leukemic cell line (HL60) in culture is accompanied by changes in acid phosphatase (Acpase) activity. The increase in activity is less than twofold when the leukemic cells are stimulated by dimethylsulfoxide (DMSO) to differentiate into metamyelocytes and granulocytes but is eightfold when the cells are stimulated by the tumor-promoting agent 12-0-tetradecanoylphorbol 13-acetate (TPA) to differentiate into macrophage-like cells. Five different isozymes of Acpase were separated by acrylamide gel electrophoresis. Isozyme 1, the most anodal isozyme, was found to be present in undifferentiated, DMSO-treated and TPA-treated cells; isozyme 2 was a very faint band observed both in DMSO- and TPA-treated cells, the isoenzymes 3a and 3b were present only in TPA-induced cells; and isozyme 4, the most cathodal isozyme, was present both in TPA- and DMSO-induced cells. A time sequence study on the appearance of the various forms after TPA treatment indicated that the expression of the isozymes is regulated in an uncoordinated fashion. Acpase activity has been shown by ultrastructural cytochemistry to be localized in the entire rough endoplasmic reticulum (RER) and in areas of the smooth endoplasmic reticulum (SER) located near the Golgi complex in differentiating cells but to be extremely weak, if at all detectable, in undifferentiated promyelocytes.

Induction of differentiation in human myeloid leukemic cells by T-2 toxin and other trichothecenes

1987 ◽  
Vol 89 (3) ◽  
pp. 418-428 ◽  
Author(s):  
Abdalrahaman Samara ◽  
Boris Yagen ◽  
Israel Agranat ◽  
Eliezer A. Rachmilewitz ◽  
Eitan Fibach
Keyword(s):  
Leukemic Cells ◽  
Induction Of Differentiation

scholarly journals Alkaloid-rich fraction of Himatanthus lancifolius contains anti-tumor agents against leukemic cells

2010 ◽  
Vol 46 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Melissa Pires de Lima ◽  
Luciana Farhat Hilst ◽  
Fernanda Vanessa Rechinbach Mattana ◽  
Cid Aimbiré de Moraes Santos ◽  
Almeriane Maria Weffort-Santos
Keyword(s):  
Annexin V ◽  
Leukemic Cell ◽  
Leukemic Cells ◽  
Main Compound ◽  
Leukemic Cell Lines ◽  
Flow Cytometric ◽  
Induction Of Differentiation ◽  
Daudi Cells ◽  
Reh Cells ◽  
Marrow Cells

The effects of the alkaloid-rich fraction of Himatanthus lancifolius (Müll. Arg) Woodson on normal marrow cells and leukemic cell lines were investigated. After 48 h exposure, the proliferation assay showed significant cell growth inhibition for Daudi (0.1-10 µg/mL), K-562 (1-10 µg/mL), and REH cells (10-100 µg/mL), yet was inert for normal marrow cells. A similar inhibition profile was observed in clonogenic assays. This alkaloid-rich fraction, in which uleine is the main compound, showed no signs of toxicity to any cells up to 10 µg/mL. Cell feature analyses after induction of differentiation showed maintenance of the initial phenotype. Flow cytometric expression of Annexin-V and 7-AAD in K-562 and Daudi cells has indicated that the cells were not undergoing apoptosis or necrosis, suggesting cytostatic activity for tumor cells

scholarly journals Induction of Differentiation in Acute Promyelocytic Leukemia Cells (HL-60) by the Verticillin Derivative Sch 52900

2002 ◽  
Vol 57 (7-8) ◽  
pp. 759-768 ◽  
Author(s):  
Gerhard Erkel ◽  
Alexandra Gehrt ◽  
Timm Anke ◽  
Olov Sterner
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Promyelocytic Leukemia ◽  
Leukemic Cells ◽  
Tetrazolium Chloride ◽  
Extracellular Signal Regulated Kinase ◽  
Molecular Events ◽  
Extracellular Signal ◽  
Blue Tetrazolium Chloride ◽  
Induction Of Differentiation ◽  
Nbt Reduction

The HL-60 cell line, derived from a patient with acute promyelocytic leukemia, is a widely used model system to study the cellular and molecular events involved in differentiation of leukemic cells. In a screening for inducers of differentiation of HL-60 cells, cultures of Gliocladium strain 4-93 were found to produce Sch 52900, a previously isolated diketopiperazine (Chu et al,. J. Antibiotics 48, 1440-1445). Sch 52900 induced the differentation of 50-69% of HL-60 cells at concentrations of 6.8-13.6 nᴍ as measured by nitro-blue tetrazolium chloride (NBT) reduction which was followed by apoptosis as shown by DNA fragmentation. Our results demonstrate that growth arrest and the induction of differentiation by Sch 52900 is due to the induction of the cell cycle inhibitor p21WAF and an inhibition of the extracellular signal-regulated kinase (ERK) signaling pathway which leads to the activation of the transcription factor AP-1.

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