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Biomedical subjects

M Hozumi

Publications and source records attributed to M Hozumi.

At least 127 records · Page 7Linked to original sources
PubMed1983

Flow cytometric analysis of unbalanced control of protein accumulation and DNA synthesis in differentiating mouse myeloid leukemia cells.

The protein and DNA contents of mouse myeloid leukemia M1 (clone B24) cells were determined by flow cytometry (FCM) after double fluorescent staining of the cells with fluorescein isothiocyanate and propidium iodide. FCM analysis showed that there was a linear relationship between the DNA and protein contents in logarithmically growing cells, although the protein content showed some variation. B24 cells can be induced to differentiate into macrophage-like cells by treatment with a protein inducer(s) in conditioned medium (CM) of hamster embryo cells. When the cells were treated with various concentrations of CM, cells with a 2C DNA content, G1/0 cells, increased and protein accumulated in these G1/0 cells. The increases in the number of G1/0 cells and in their protein content per cell were proportional to the concentration of CM. Serial analysis of changes in the contents of DNA and protein in differentiating B24 cells showed that DNA synthesis was suppressed by differentiation-induced block of the cell cycle at the G1/0 phase, whereas increase in the protein content was not completely suppressed by block of the cell cycle. These results suggest that unbalanced control of the DNA and protein contents of B24 cells is involved in the mechanisms of the morphological changes during differentiation into macrophages.

Animals↗
PubMed1983

Possible differentiation of human acute myeloblastic leukemia cells by daily and intermittent administration of aclacinomycin-A.

A rapid decrease of myeloblasts and a remarkable increase of mature neutrophils, mostly with Pelger anomaly, were observed in the peripheral blood of a 51-year-old woman with terminal acute myeloblastic leukemia during 16 days of daily i.v. administration of 20 mg aclacinomycin-A (ACM-A). When the same dose was administered later on three consecutive days each week, a similar hematore neutrophils, mostly with Pelger anomaly, were observed in the peripheral blood of a 51-year-old woman with terminal acute myeloblastic leukemia during 16 days of daily i.v. administration of 20 mg aclacinomycin-A (ACM-A). When the same dose was administered later on three consecutive days each week, a similar hematore neutrophils, mostly with Pelger anomaly, were observed in the peripheral blood of a 51-year-old woman with terminal acute myeloblastic leukemia during 16 days of daily i.v. administration of 20 mg aclacinomycin-A (ACM-A). When the same dose was administered later on three consecutive days each week, a similar hematological change occurred again. An increase of myeloblasts observed between the third and the fifth week of this intermittent schedule was accompanied by that of mature neutrophils. Thrombopenia and anemia did not improve significantly. These findings may indicate the induction of leukemic myeloblasts by ACM-A into mature neutrophils. Administration of relatively small dose anthracyclines including ACM-A may be another potential choice in the treatment of refractory acute non-lymphocytic leukemia (ANLL) or ANLL after relapse.

Aclarubicin↗
PubMed1983

Effects of inducers of erythroid differentiation of human leukemia K562 cells on vincristine-resistant K562/VCR cells.

K562/VCR cells, which are resistant to the cytotoxicity of vincristine, were isolated from human erythroleukemia K562 cells. Various compounds that induce erythroid differentiation of K562 cells were tested on K562/VCR cells. Differentiation of K562/VCR cells was not induced by actinomycin D or adriamycin alone, but the resistance of these cells to the inducers was overcome by verapamil. In contrast, mitomycin C, butyric acid and hemin induced differentiation of K562/VCR cells as effectively as that of K562 cells. These results suggest that therapy by induction of differentiation of leukemic cells is effective for leukemic cells that have acquired resistance to therapeutic drugs.

Animals↗
PubMed1983

Acidic isoferritins do not suppress differentiation of mouse myeloid leukemic M1 cells.

The differentiation of mouse myeloid leukemia line cells (M1) into macrophages or granulocytes has been reported. Resistant M1 cells which did not differentiate even with a high concentration of inducer of differentiation were isolated from M1 cells. The conditioned medium of the resistant M1 cells (RCM) inhibited the induction of differentiation of M1 cells and the formation of macrophage and granulocyte colonies of normal mouse bone marrow cells. Acidic isoferritins known as negative regulators of normal bone marrow cells (CFU-GM) failed to inhibit the induction of differentiation and growth of M1 cells. The RCM treated with anti-acidic isoferritin serum could inhibit the induction of differentiation of M1 cells as did the untreated RCM. The activities, in RCM, inhibiting growth and differentiation of the normal bone marrow cells were partly neutralized by treatment with the antiserum but most of the activities remained. These results suggest that growth and differentiation of the mouse myeloid leukemia M1 cells are not regulated by acidic isoferritins and other inhibitory activities affecting normal bone marrow colony formation, in addition to acidic isoferritins, are released from M1 cells.

Animals↗
PubMed1983

Prolongation by interferon preparation of the survival time of mice implanted with differentiation-inducible mouse myeloid leukemia cells.

The effect of L-cell interferon (IFN) preparation on the survival times of mice implanted with two different clones (T-22 and R-4) of mouse myeloid leukemic M1 cells were examined. T-22 cells, but not variant R-4 cells, can be induced to differentiate in vitro or in vivo into macrophages and granulocytes. In vitro growth of R-4 cells was markedly suppressed by IFN, but that of T-22 cells was resistant to IFN. The survival times of mice with implanted T-22 cells were prolonged by treatment with IFN but those of mice with implanted R-4 cells were not.

Animals↗
PubMed1983

Induction of differentiation of human acute non-lymphocytic leukemia cells in primary culture by inducers of differentiation of human myeloid leukemia cell line HL-60.

Leukemia cells from patients with acute non-lymphocytic leukemia were treated with various inducers of differentiation of the human promyelocytic leukemia cell line HL-60. All cells in 14 specimens tested underwent morphological, functional and histochemical changes after treatment with some inducers of differentiation of HL-60 cells, but the most effective inducer varied for different specimens. These results suggest that treatment with some inducers should be effective for inducing most acute myeloid leukemia cells to differentiate into morphologically and functionally mature granulocytes and macrophages.

Adult↗
PubMed1983

1 alpha,25-Dihydroxyvitamin D3 and 1 alpha-hydroxyvitamin D3 prolong survival time of mice inoculated with myeloid leukemia cells.

Syngeneic SL mice inoculated with murine myeloid leukemia cells (M1) all died of leukemia within 30 days. Treatment three times a week with 12.5-50 pmol per mouse of either 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3], the active form of vitamin D3, or its synthetic analog, 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3], considerably prolonged the survival time of mice inoculated with M1 cells. 1 alpha(OH)D3 was more effective than 1 alpha,25(OH)2D3 in increasing the survival time of the mice. 1 alpha(OH)D3 also increased the survival time of nude mice inoculated with M1 cells. The 1 alpha(OH)[3H]D3 administered intraperitoneally to tumor-bearing mice was converted very rapidly to 1 alpha,25(OH)2-[3H]D3. The chronic administration of 25 pmol of 1 alpha(OH)D3 to tumor-bearing mice for 30 days caused no appreciable hypercalcemia. These results indicate clearly that 1 alpha,25(OH)2D3 is effective not only in inducing differentiation of M1 cells in vitro, as previously reported [Abe, E., Miyaura, C., Sakagami, H., Takeda, M., Konno, K., Yamazaki, T., Yoshiki, S. & Suda, T. (1981) Proc. Natl. Acad. Sci. USA 78, 4990-4994], but also in prolonging the survival time of mice inoculated with M1 cells.

Animals↗
PubMed1983

[Chemoprevention of carcinogenesis].

Inhibitors and their mechanisms of inhibition of various processes in chemical carcinogenesis, metabolic activation of chemical carcinogens followed by initiation and promotion in chemical carcinogenesis are reviewed. Furthermore, significance of the inhibitors of chemical carcinogenesis in foods and food additives and problems of side effects of these inhibitors are discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1983

Effect of mouse interferon on growth and differentiation of mouse bone marrow cells stimulated by two different types of colony-stimulating factor.

The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony-stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.

Animals↗
PubMed1983

[Cellular actions of inhibitors of chemical carcinogenesis: modifications of syntheses of prostaglandins and differentiation of myeloid leukemia cells].

Although various substances are involved in modification of chemical carcinogenesis, prostaglandins have been known to play an important role in the modification of the carcinogenesis. In this report, recent advances in the modification of chemical carcinogenesis by prostaglandins are reviewed. In addition, recent experimental results on the modification of cell differentiation by prostaglandins and some inhibitors of chemical carcinogenesis are described. Some inhibitors of chemical carcinogenesis are found to modify differentiation of mouse myeloid leukemia cells (M1) into macrophages and granulocytes by perturbation of syntheses of prostaglandins. These experimental results suggest that the modification by the inhibitors of carcinogenesis of differentiation of cells by perturbation of syntheses of prostaglandins is involved in the mechanisms of inhibition of chemical carcinogenesis.

Animals↗
PubMed1983

Increased synthesis of hyaluronic acid by mouse mammary carcinoma cell variants with high metastatic potential.

Variant subpopulations of FM3A mouse mammary carcinoma cells that have increased lung-colonizing potential were obtained previously by sequentially harvesting pulmonary metastases, culturing their cells in vitro, and reestablishing the metastases in vivo. In the present study, glycosaminoglycan production by the parental and variant cells was studied after metabolic labeling of cultures by [14C]glucosamine for 24 hr. Analysis of the products indicated that the rate of incorporation of the labeled precursor into hyaluronic acid in the high-metastatic variant cells was 27 to 54 times the rate in the low-metastatic variant cells and that the increase in hyaluronic acid synthesis was not associated with an increase in the rate of synthesis of other glycosaminoglycans. Both the cell layers and media of high-metastatic variants contained a much higher proportion of radioactivity in hyaluronic acid than did the corresponding fractions of low-metastatic cell lines. The results provide a basis for further investigation of the potential role of hyaluronic acid in control of the behavior of epithelial tumor cells during metastasis.

Animals↗
PubMed1982

Modification of membrane phospholipid composition by choline analogues induces differentiation of cultured mouse myeloid leukemia cells.

Mouse myeloid leukemia M1 cells could be induced by various inducers to form Fc receptors, phagocytize, produce lysozyme, and change into forms that were morphologically similar to macrophages and granulocytes. Previous experiments showed that change in phospholipid metabolism was associated with cell differentiation. In the present experiment, culture of M1 cells with choline analogs such as N-monomethyl-ethanolamine and N,N'-dimethylethanolamine resulted in accumulation of phosphatidyl-N-monomethyl-ethanolamine and phosphatidyl-N,N'-dimethylethanolamine in the cell membranes. This change upon treatment with choline analogs was associated with morphological and functional differentiation of the M1 cells into macrophages and granulocytes. These results suggest that phospholipid metabolism is involved in the mechanism of differentiation of M1 cells.

Animals↗
PubMed1982

Differentiation of isotope-labeled myeloid leukemia cells free in the peritoneal cavity of syngeneic mice.

Ml cells were labeled in vitro with [3H]thymidine and injected into the peritoneal cavity of syngeneic mice. After several days the peritoneal cells were harvested and [3H]labeled cells were determined by autoradiography. The inoculated isotope-labeled Ml cells differentiated in the peritoneal cavity and lipopolysaccharide, an inducer of cell differentiation, significantly stimulated differentiation. These results provide direct evidence that Ml cells can be induced to differentiate in vivo under conditions in which leukemia can develop.

Animals↗
PubMed1982

Inhibition of differentiation of mouse myeloid leukemia cells by heat-stable calf serum components of very high molecular weight.

Mouse myeloid leukemia cells (Ml) were induced to differentiate into macrophages and granulocytes by various inducers including glucocorticoid. The tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited the induction of differentiation of Ml cells in medium containing calf serum, but enhanced the induction in medium containing fetal calf serum and several inducers. For elucidation of the factor(s) in serum affecting the response of Ml cells to tumour promoters, calf serum was fractionated by Sephadex G-200 gel filtration. Differentiation of Ml cells induced by dexamethasone was markedly inhibited by TPA and high mol. wt fractions of calf serum eluted in the void volume and low mol. wt fractions that co-migrated with bovine serum albumin. High mol. wt fractions alone inhibited the differentiation of Ml cells induced by dexamethasone, and also acted additively with TPA in inhibiting the differentiation. The inhibition by high mol. wt fractions was not related to cytotoxicity and was reversible. The differentiation of Ml cells induced by proteinous inducer or lipopolysaccharide was also inhibited by high mol. wt fractions. The inhibitory factor was heat stable (70 degrees C for 20 min or 90 degrees C for 10 min). These results suggest that the tumour promoter and calf serum components cooperate in inhibiting differentiation of mouse myeloid leukemia cells induced by various inducers.

Animals↗
PubMed1982

Interferon production in mixed cultures of mouse spleen cells and tumor cells: IFN-gamma as the main component.

Interferon (IFN) production in mixed cultures of mouse spleen cells and tumor cells was investigated, mainly using mouse myeloid leukemic cells, M1, and spleen cells from syngeneic SL mice. Spleen cells from other mouse strains (C57BL/6, BALB/c nude and C57BL/6 beige) and other tumor cells (L929 and YAC-1) were similarly effective for IFN production, but mouse mammary carcinoma FM3A cells were not. As the IFN-inducing stimulus, mycoplasma contaminating the tumor cells, or endogenous retrovirus in them, may possibly be involved. The type of IFN produced was identified as IFN-gamma as a major component and IFN-alpha and -beta as minor ones, by acid stability tests and neutralization by antisera with defined specificities against alpha, beta, and gamma. Depletion of natural killer cells from spleen cells did not appreciably affect IFN production, but depletion of Thy 1.2 antigen-bearing cells greatly reduced IFN-gamma production, indicating that T cells were the main IFN producers.

Animals↗