Showing papers on "Friend leukemia published in 1982"
TL;DR: The finding that Interferon was equally effective in mice inoculated with interferonresistant cells as in mice innoculated withinterferon‐sensitive cells suggests that in this experimental systemInterferon does not act directly on the tumor cells, but that the interferOn‐induced antitumor activity is mediated by the host.
Abstract: Interferon-sensitive (745) and interferon-resistant (3Cl-8) Friend leukemia cells (FLC) are highly tumorigenic for DBA/2 mice. The phenotype of interferon sensitivity or resistance does not change with in vivo passage. Daily administration of mouse interferon markedly enhanced the survival time of mice injected with either 745 or 3Cl-8 cells. Use of quantitative methods for determining the number of FLC (colony formation in agarose and immunofluorescence) permitted us to show that potent, partially purified or highly purified mouse interferon (s.a. 0.5 to 1 × 109 u/mg protein) induced a 100- to 1,000-fold decrease in the number of tumor cells in the peritoneal cavity in the days following inoculation of 745 or 3Cl-8 cells. Interferon decreased the number of FLC even when treatment was initiated at a time when tumor cells were multiplying exponentially in the peritoneal cavity. There was no evidence that interferon acted as an inducer of FLC differentiation in vivo. The finding that interferon was equally effective in mice inoculated with interferonresistant cells as in mice inoculated with interferon-sensitive cells suggests that in this experimental system interferon does not act directly on the tumor cells, but that the interferon-induced antitumor activity is mediated by the host.
116 citations
TL;DR: Proton nuclear magnetic resonance of intact Friend leukemia cells was used to analyze their erythroid-like differentiation, and a dramatic signal change was attributed to a fourfold increase in cytoplasmic phosphorylcholines.
Abstract: Proton nuclear magnetic resonance of intact Friend leukemia cells was used to analyze their erythroid-like differentiation. The technique, which requires only 10(3) to 10(9) cells and approximately 2 minutes for acquisition of each spectrum, demonstrated the occurrence of many signal changes during differentiation. With cell extracts, 64 signals were assigned to 12 amino acids and 19 other intermediary metabolites, and a dramatic signal change was attributed to a fourfold increase in cytoplasmic phosphorylcholines.
101 citations
TL;DR: It is suggested that interferon induces a host‐mediated antitumor effect by mechanisms which are not mediated by easily recoverable soluble factors or by cytotoxic cells.
Abstract: We have attempted to determine what host mechanisms are responsible for inducing a rapid decrease in the number of Friend leukemia cells (FLC) in the peritoneal cavity of interferon-treated mice. By injecting radiolabelled FLC, we showed that there was a greater loss of radioactivity from individual interferon-treated mice than from control mice. Thus, it was likely that fewer cells were recovered from the peritoneal cavity of interferon-treated mice because of cell destruction. Treatment of mice with interferon limited to the period preceding tumor-cell inoculation conferred some degree of antitumor activity, although this regimen was far less effective than when interferon treatment was initiated and continued daily after tumor-cell inoculation. We have been unable to transfer any antitumor activity with peritoneal washings containing macrophages and lymphocytes from interferon-treated donor mice to tumor-inoculated recipient mice. Inoculation of silica particles i.p., which destroys macrophage function and may affect NK cell activity, did not abrogate interferon's antitumor activity. We suggest that interferon induces a host-mediated antitumor effect by mechanisms which are not mediated by easily recoverable soluble factors or by cytotoxic cells. The nature of this potent interferon-induced host mechanism remains unknown.
62 citations
TL;DR: Analysis of leukemias indicated that they are multistage diseases, and studies of the hemopoietic modulations indicated that mice that developed early or late erythroleukemia had dramatic increases in erythyroid bursts, suggesting that the leukemic blocks are at the level of BFU-E or earlier.
47 citations
Journal Article•
TL;DR: Nuclear outward transport and deglycosidation were inhibited by sodium azide and low temperatures; this suggests that they are regulated by an active transport process and by an enzymatic activity, respectively.
Abstract: The kinetics of uptake by cells and nuclear incorporation of aclacinomycin A was studied in Friend leukemia cells. It was shown that uptake is a very rapid process. The intracellular concentration is maximum in 10 min and mainly (about 75%) localized in the nucleus. Most of the incorporated drug will disappear from the cell by a two-step mechanism: (a) efflux from the nucleus to the cytoplasm; and (b) deglycosidation at C-7 to the alkavinone form in the cytoplasmic fraction. The cellular uptake was temperature dependent but was not prevented by sodium azide treatment. We assumed, therefore, that it is related to the composition and to the dynamic structure of the cell surface membrane. Nuclear outward transport and deglycosidation were inhibited by sodium azide and low temperatures; this suggests that they are regulated by an active transport process and by an enzymatic activity, respectively.
16 citations
TL;DR: It is concluded that erythroid differentiation induced by DMSO is related to changes in the lipid components of FLC membranes.
15 citations
TL;DR: The findings indicate that erythrodifferentiation induced by DMSO results in a variety of changes in the lipid composition of the membranes of Friend leukemia cells.
Abstract: The effects of dimethyl sulfoxide (DMSO)-induced differentiation of Friend leukemia cells in vitro on the lipid composition of these cells have been examined DMSO had no early effect on the incorporation of either [14C]glycerol or [3H]methyl choline chloride into the total lipids or individual phospholipids of Friend cells up to 240 min after addition of the inducer Examination of DMSO-differentiated Friend cell phospholipids revealed a percentage composition which was similar to control cells, with phosphatidylcholine and phosphatidylethanolamine in both uninduced and differentiated cells accounting for over 75% of the total phospholipid Sphingomyelin levels were significantly lower in Friend cells than in normal adult mouse erythrocytes, and differentiation of murine erythroleukemia cells resulted in a further lowering of this phospholipid In contrast, a significant increase in the level of phosphatidylethanolamine occurred as a result of maturation Fatty acid analysis of major lipid classes of differentiated Friend cells showed significant reduction in saturation, but no alteration in chain length in comparison to undifferentiated cells A pronounced decrease in the cellular content of both free and esterified cholesterol, which resulted in a 45% decrease in the ratio of cholesterol/phospholipids, occurred in cells differentiated by the polar solvent The findings indicate that erythrodifferentiation induced by DMSO results in a variety of changes in the lipid composition of the membranes of Friend leukemia cells
13 citations
TL;DR: The action of 12-O-tetradecanoylphorbol-13-acetate on several retrovirus-related functions was investigated in four virus-host cell systems and TPA inhibited the induction of endogenous virus formation in B cell mitogen-stimulated spleen cell cultures from BalbC mice.
Abstract: The action of 12-O-tetradecanoylphorbol-13-acetate (TPA) on several retrovirus-related functions was investigated in four virus-host cell systems. The following effects were recorded: (i) in STU-mice, infected with the Friend virus complex (Friend) murine leukaemia virus/Friend spleen focus forming virus) and treated with TPA (50 ng/g) for one week prior to infection, the number of spleen foci increased 5-fold over the control. (ii) Addition of TPA (0.04 to 40 ng/ml) to virus-producing cell systems resulted in a 2-fold increase of extracellular reverse transcriptase activity. The maximum response was observed in Friend leukemia virus-producing mouse cells at 0.1 to 0.4 ng TPA/ml and in simian sarcoma virus-producing rat cells at 4 ng/ml. (iii) The efficiency of transformation of BalbC 3T3 cells by Moloney murine sarcoma virus, tested in a focus formation assay, was slightly enhanced by TPA. (iv) TPA inhibited the induction of endogenous virus formation in B cell mitogen-stimulated spleen cell cultures from BalbC mice.
8 citations
TL;DR: This method is simpler than any previously reported methods, and is sufficiently reliable to use in determining hemoglobin in living cells as a quantitative marker of erythroid differentiation.
Abstract: The potencies of poly(ADP-ribosylation)-inhibitors in inducing erythroid differentiation of Friend erythroleukemia cells were surveyed. Picolinamide and m-aminobenzamide were newly found to be inducers, whereas compounds related caffeine did not induce differentiation. In other series of experiments some bile acids suspected of being tumor promoters were found to inhibit the differentiation like typical tumor promoters such as phorbol esters. These modifications of erythroid differentiation were detected by an opal glass transmission method. This method is simpler than any previously reported methods, and is sufficiently reliable to use in determining hemoglobin in living cells as a quantitative marker of erythroid differentiation.
7 citations
Journal Article•
TL;DR: In two of the animals with the FLC neoplasia the disease manifestation is an erythroid leukemia similar to the one obtained directly with the virus in normal DBA/2 mice.
Abstract: SUMMARY To test the ability of cloned committed erythroleukemic cells to participate in development we have injected Friend leukemia cells (FLC) into C57B1/6 mouse blastocysts together with Friend leukemia virus (FLV) and we have examined the newborn individuals derived from them. Five animals out of 32 born have FLC-derived neoplasia. The incidence of neoplasia is increased as compared with other similar experiments without the virus. In two of the animals with the FLC neoplasia the disease manifestation is an erythroid leukemia similar to the one obtained directly with the virus in normal DBA/2 mice.
2 citations
TL;DR: Butyrated hydroxyanisole was found to inhibit the appearance of benzidine-positive cells in cultures of Friend leukemia cells treated with the inducers, but did not affect the induction of globin or globin mRNA accumulation.
TL;DR: Experiments with Friend and Daudi cells indicated that a number of changes in membrane transport occur rapidly after the addition of interferon to sensitive cells, and a piretanide-inhibitable Na+,K+, 2Cl- co-transport system was specifically inhibited afterInterferon treatment of sensitive cells.
Abstract: The Friend murine erythroleukemia cell system and the Daudi Burkitt's lymphoma cell system were used to study the effect of growth-inhibitory concentrations of interferon on membrane functions. Experiments with Friend-cell clones sensitive and resistant to interferon indicated that a number of changes in membrane transport occur rapidly after the addition of interferon to sensitive cells. While no change was observed in the activity of the (Na+/K+)ATPase in Friend cells sensitive or resistant to interferon, a piretanideinhibitable Na+,K +, 2C1- co-transport system was specifically inhibited after interferon treatment of sensitive cells. In contrast) treatment of Daudi cells with purified molecularly cloned or standard preparations of human leukocyte interferon gave rise to no early changes in the transport of amino acids, 32P i, sugars, or 86Rb+. The major change observed in Daudi cells was a marked reduction in the uptake and incorporation of thymidine, which begins to decrease after 8-10 h of exposure to interferon. In addition to the ability of interferon to inhibit the replication of cytocidal viruses at the level of translation, interferons inhibit the release of membrane budding viruses, cell growth, and differentiation. The interferon-induced anti-proliferati ve effect has been shown to be an intrinsic property of the interferon molecule, in that molecularly cloned, HPLC-purified human leukocyte interferons inhibit cellular proliferation. Evidence from our laboratory and others indicates that alterations in the cell membrane are involved in interferon-media ted inhibition of cell growth (for review see i).
TL;DR: A clone of Friend leukemia (FL) cells has been isolated which, in the presence of hexamethylene bisacetamide (HMBA) as inducer, is capable of growing and producing heme for long periods of time.