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Friend leukemia
About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.
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TL;DR: It is suggested that resistant is the consequence of changes induced in the plasma membrane components that may differ according to which drug is used.
Abstract: Based on the fluorescence properties of adriamycin (ADM) and daunorubicin (DNR), uptake in sensitive and resistant Friend leukemia cells (FLC) was studied with the aid of the fluorescence activated cell sorter (FACS II). A quantitative cell by cell fluorescence intensity analysis showed a differential affinity of FLC to ADM and DNR. The cellular uptake of these two drugs was temperature dependent and was not hindered by sodium azide treatment; incorporation into isolated nuclei was not temperature dependent, nor hindered by sodium azide. Friend leukemia cell variants resistant to adriamycin (ADM-RFLC) and to daunorubicin (DNR-RFLC) were developed. The rate of uptake of ADM and DNR across the plasma membrane of these two cell variants was lower than in sensitive cells. Although these cells were crossresistant to both ADM and DNR, the drug-induced fluorescence intensity was distributed differently in the corresponding resistant cell variants. We suggest therefore that resistant is the consequence of changes induced in the plasma membrane components. These changes may differ according to which drug is used.
35 citations
TL;DR: There appears to be a functional similarity between this inhibitor from Friend leukemia cells and the hemin-controlled repressor from reticulocytes.
35 citations
TL;DR: Interferon inoculated intraperitoneally diffused from the peritoneal cavity into the circulation at a relatively constant rate and a significant level of interferon was maintained in the serum for as long as 5 hours.
Abstract: SummaryVarious factors pertaining to the absence of interferon in the tissues of mice with Friend disease and the passive administration of interferon to mice with Friend disease have been investigated.The diffusion of interferon after intravenous and intraperitoneal inoculation has also been described. After intravenous inoculation the titer of interferon in the serum decreased markedly and interferon was recovered in the urine. Interferon inoculated intraperitoneally diffused from the peritoneal cavity into the circulation at a relatively constant rate and a significant level of interferon was maintained in the serum for as long as 5 hours.We gratefully acknowledge the excellent assistance of Mlle. Chantal Bourali and of Mlle. Marie-The rese Thomas.
33 citations
TL;DR: Mice pretreated with complete Freund's adjuvant had an enhanced resistance to autochthonous and transplanted tumors and it is suggested that host resistance to intracellular infectious agents and neoplasia is related in a fundamental way and the activated macrophage is a common effector arm for expression of this resistance.
Abstract: SummaryMice pretreated with complete Freund's adjuvant had an enhanced resistance to autochthonous and transplanted tumors. Delayed time to death and/or increased survival was noted in CFA pretreated mice grafted intraperitoneally with Sarcoma 180, leukemia L1210, or Friend leukemia spleen cells. In addition, CFA pretreatment caused a statistically significant delay in spontaneous mammary tumor development in C3H/HeJ mice and spontaneous leukemia in AKR mice. We propose that host resistance to intracellular infectious agents and neoplasia is related in a fundamental way and the activated macrophage is a common effector arm for expression of this resistance. It is also suggested that a nonimmunologic growth control mechanism such as we have described offers a rapid acting homeostatic process for destruction of cells with abnormal growth properties in vivo.
33 citations
TL;DR: It is demonstrated that SFFVp alone can alter the growth characteristics of erythroid progenitors and is directly responsible for the induction of vBFU-E in vitro and the erythyroid hyperplasia in vivo.
Abstract: The polycythemia-inducing strain of Friend virus (FV-P) causes a multistage erythroleukemia in susceptible mice. FV-P is a complex of two viruses, a replication-competent virus [Friend murine leukemia virus (F-MuLV)] and a replication-defective spleen focus-forming virus (SFFVp). We have addressed directly the role of SFFVp in the induction of the early stages of Friend disease by constructing stocks of SFFVp free of detectable F-MuLV, using a recently described retroviral helper-cell line. These preparations are capable of inducing erythroid bursts (vBFU-E) whose inducibility, kinetics, and responsiveness to erythropoietin suggest that they are very similar, if not identical, to the vBFU-E induced by FV-P. Single injections of helper-free SFFVp had no apparent effects in vivo, although the addition of exogenous helper virus to the inoculum resulted in the induction of classic Friend disease. Increasing the effective titer by giving mice five daily virus injections resulted in the induction of splenomegaly and a large increase in the number of erythroid colony-forming units that were independent of erythropoietin. When the injections were discontinued, the spleens regressed and all the mice survived. When the injections were continued, all the mice died within 25 days of the first injection. These results demonstrate that SFFVp alone can alter the growth characteristics of erythroid progenitors and is directly responsible for the induction of vBFU-E in vitro and the erythroid hyperplasia in vivo. They also demonstrate that the initial polyclonal stage of Friend disease is reversible and can be reproduced by using preparations of SFFVp free of detectable F-MuLV.
32 citations