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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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Journal ArticleDOI
TL;DR: An endonuclease activity shown to be associated with Friend leukemia virus has been characterized using double-stranded phi X174 DNA as substrate, and when Mn2+ was substituted for Mg2+ in the reaction mixture, the number of nicks introduced into circular DNA duplexes by the virus associated end onuclease was greatly increased.

7 citations

Journal ArticleDOI
TL;DR: The results on the estimation of globin mRNA content in the cytoplasm and nuclei of induced cells indicated that in all the phenotypic variants tested, the transcriptional activation of Globin genes is primarily involved in the induction of globIn synthesis rather than the alteration in the translational, or post-transcriptional events.

7 citations

Journal ArticleDOI
TL;DR: Hamster-adapted Friend murine leukemia virus infected hamster cells and produced an XC-positive progeny in vitro, but the sensitivity of hamster- Adapted F-MuLV's to Hamster cells was about 100 times lower than that to mouse cells.
Abstract: Hamster-adapted Friend murine leukemia virus (F-MuLV) infected hamster cells and produced an XC-positive progeny. However, the sensitivity of hamster-adapted F-MuLV's to hamster cells was about 100 times lower than that to mouse cells. Hamster cells chronically infected with F-MuLV in vitro produced progeny virus in titers comparable to those in similarly infected mouse cells. Xenotropic and amphotropic murine leukemia virus can infect hamster cells when phenotypically mixed with the F-MuLV. Murine sarcoma virus pseudotyped with the F-MuLV easily induced sarcomas in hamsters and transformed hamster cells in vitro.

7 citations

Journal Article
TL;DR: In this paper, a passive transfer of sensitized T-cells from regressing FV immunized or regressed mice caused regression of the conventional lethal leukemia induced by FV. This model thus provides an experimental system of highly effective passive cellular immunotherapy against an autochthonous, fully developed leukemia.
Abstract: The erythroleukemia induced in susceptible mice by Friend virus (FV) is a progressive, lethal disease. A variant strain of Friend virus (regressing FV) produces a histopathologically identical leukemia except that the disease spontaneously regresses in 50% of leukemic mice. Normal T-cell and macrophage function are required for regression to occur and in animals that are going to regress, specifically reactive T-cells are found in the spleen. Passive transfer of sensitized T-cells from regressing FV immunized or regressed mice caused regression of the conventional lethal leukemia induced by FV. To expand the effector cell populations, characterize them and improve their therapeutic efficacy, sensitized T-cells were cultured in vitro . The T-cells, isolated from regressed or immunized mice, were grown and expanded in vitro with interleukin 2 and antigen (mitomycin C treated regressing FV-infected cell lines). The T-cells demonstrated high levels of in vitro cytotoxicity against FV antigens but exhibited no blastogenic response to the same antigens. When fully FV-induced leukemic mice (14 days post virus inoculation; spleen weight, >0.75 g) were given one injection of 5 × 106 in vitro cultured T-cells and no other treatment the mice experienced permanent regressions of their disease. From T-cell cultures depleted of specific cell populations with monoclonal antisera, helper Lyt-1+ cells were shown to be responsible for permanent regressions (cures), whereas cytotoxic Lyt-2+ cells caused temporary leukemia remissions. This model thus provides an experimental system of highly effective passive cellular immunotherapy against an autochthonous, fully developed leukemia, requiring no adjunctive treatment for activity.

7 citations

Journal ArticleDOI
TL;DR: These studies strongly suggested that the stromal cells of the spleen are not directly involved in the virus-induced leukemic process but acted as supporting structure for the malignant cells.
Abstract: Pieces of Friend leukemic spleens implanted sc into mice regenerated into normal-appearing spleens if animals were protected against the leukemia. In unimmunized animals, the implant regenerated normally, but was subsequently infiltrated by leukemia cells. This leukemia cell infiltration required at least 30% stromal regeneration of the implant. The hematopoietic regeneration was primarily a repopulation with cells from the host animal, not with cells indigenous to the donor spleen. The development of the implant, whether normal or leukemic, was retarded by the presence of the host spleen, whether leukemic or normal. These studies strongly suggested that the stromal cells of the spleen are not directly involved in the virus-induced leukemic process but acted as supporting structure for the malignant cells.

7 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20213
20192
20161
20151
20143
20121