Friend leukemia

About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.

Water permeability changes studied by 17O nuclear magnetic resonance during differentiation of Friend leukemia cells.

Abstract: Water permeability of Friend leukemia cells was studied by 17O nuclear magnetic resonance during differentiation induced by dimethyl sulfoxide (Me2SO). While in noninduced cells water permeability was essentially constant during the growth period, in the Me2SO-induced cells there were two distinct periods at which the water permeability was increased by at least an order of magnitude. These periods correspond to approximately one doubling time and 6 days of growth. This change in water permeability is not due to direct interaction of Me2SO with the membrane but must be ascribed to structural changes in the membrane during the course of differentiation.

Effect of the nitrosourea derivative rpcnu (ICIG 1163) on the development of Friend leukemia in mice.

Abstract: Friend leukemia was used as an experimental model to study the action of a ribofuranosyl derivative of nitrosourea : RPCNU. This new product was known to be active in L 1210 leukemia and immunosuppressive. RPCNU significantly decreases the splenomegaly induced in DBA2 mice by Friend virus when it is given at a time ranging from 7 days before to 14 days after virus inoculation. The survival time in leukemic treated groups is also greatly increased. However, viral content of the spleen extracts of the leukemic treated mice is not reduced. Therefore, RPCNU cannot be considered as an antiviral agent. A comparison between survival of leukemic and non leukemic mice treated with different doses show that the effectiveness of RPCNU is correlated with its toxicity. The effect of RPCNU on Friend leukemia by cytotoxicity on hematopoietic stem cells is discussed in this paper.

Restoration of Antibody Responsiveness by Endotoxin in Retrovirus-Immunodepressed Mice: Role of Macrophages

Abstract: Exogenous retroviruses are the cause of severe immunodeficiency syndromes in humans and animals (4). Studies in our laboratory have focused on elucidating the mechanisms underlying the immunodeficiency induced in mice by retroviruses of the Friend leukemia complex (FLC). The pathologies produced by the two viral components of this complex are considerably different. Genetically susceptible mice inoculated with the entire FLC develop a rapidly progressing erythroblastosis of the spleen followed by erythroleukemia within a few weeks postinfection—a series of changes thought to be initiated by the rapidly transforming replication-defective spleen focus-forming virus. In contrast, the slow transforming replication-competent helper virus (F-MuLV), when injected alone into the same strains of mice, causes leukemias of varied histotype after a latency of several months, the only change noticeable during the long incubation period being a slight hyperplasia of the spleen (11,32).

Treatment of murine interferon-α/β-sensitive and -resistant Friend leukemia cells with tumor necrosis factor in combination with murine interferon-α/β or -γ

Abstract: Interferon-α/β (IFN-α/β)-sensitive (FLC 745) and -resistant (FLC 3C18) Friend leukemia cells (FLC) were fairly refractory to the cytotoxicity of murine tumor necrosis factor (MuTNF) in vitro. Both lines became highly sensitive to mTNF when treated in combination with murine IFN-γ; when treated with IFN-α/β, only the FLC 745 became sensitive to MuTNF. Romeo et al.(9) have reported previously that an antiviral state was induced in both FLC lines by IFN-γ, but only in FLC 745 by IFN-α/β. The present results suggest that the sensitivity to the synergistic cytotoxic effect of IFN and TNF in these cells is correlated with the ability to be induced into an antiviral state.