Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In contrast to cultured erythroleukemic cells transformed by Friend leukemia virus, in the cultured erythroleukemic murine cells transformed by Rauscher leukemia virus, the synthesis of haemoglobin cannot be induced after treatment with 1--2% dimethylsulfoxide, actinomycin D and proteolytic enzymes. Study of disturbances in the haemoglobin synthesis in this cell culture revealed that globin 9S-mRNA is either absent or present in negligible amounts in the culture. The data obtained suggest that the disturbances in haemoglobin synthesis occur at the level of transcription or processing of globin mRNA, rather than at the level of translation.
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PMID:[Synthesis of globin mRNA in cultured murine erythroleukemic cells, transformed by Rauscher leukemia virus]. 39 37

An increase in the DNAase 1 activity in the serum and an increase in the DNAase inhibitor activity in the spleen in the development of virus Friend leukemia were demonstrated. Increased activity of the inhibitor in the spleen was also revealed after intravenous injection of exogenous DNAase 1 into mice. A potential role of serum DNAase 1 in the development of experimental leukemia is discussed.
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PMID:[Possible role of DNAse I in the development of experimental leukemia]. 49 83

A latent form of persistent infection can be established in susceptible adult mice inoculated with a preparation of defective Friend spleen focus-forming virus (SFFV) purified free from standard leukemia-inducing helper virus (LLV-F). SFFV persistence was initially observed using an in vivo rescue technique in which SFFV could be directly rescued to form splenic foci of malignant erythropoiesis in mice. At approximately 30 d after virus inoculation however, SFFV could not be rescued after inoculation of LLV-F indicating that persistently infected (i.e., SFFV+) mice were either immume to exogenous helper virus or able to express SFFV-associated defective-interfering (DI) function(s). Persistent infection by SFFV was further documented using an in vitro rescue technique and ultimately resulted in the induction by SFFV of erythroleukemia in the absence of polycythemia or overt virus production. However, SFFV rescued by LLV-F from persistently infected normal and transformed hemopoietic cells was able to induce polycythemia in adult mice suggesting that this is a helper controlled property of the Friend virus complex. Transplantable SFFV-induced erythroleukemic cells could be retrieved from persistently infected yet histologically normal mice. The duration of SFFV persistence in normal spleen tissue suggests that the SFFV provirus resides in either a long-lived or pluripotent hemopoietic cell. Further, certain changes occurred, presumably in the membranes of persistently infected cells, which preceded the overt development of Friend leukemia and facilitated the definition of an SFFV preleukemic phase. Cell surface alterations were revealed using cell transfer techniques. Hemopoietic cells harboring a rescuable SFFV failed to proliferate when inoculated into lethally irradiated, syngeneic adult mice. In contrast, the transformed progeny of preleukemic cell populations and spleen cells transformed by FV complex (i.e., cells replicating both SFFV and LLV-F) were not rejected. This result suggests that histologically normal SFFV+ preleukemic cells express an antigen recognition site which is not present on overtly transformed cells and which may be a pertinent surveillance target for host anti-leukemogenic reactions.
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PMID:Persistence and pathogenicity of defective Friend spleen focus-forming virus. Decreased transplantability of hemopoietic cells as a marker for preleukemic change. 76 97

Tissue-culture-passaged, Friend leukemia virus (FV)-induced reticulum cell sarcomas from BALB/c mice (FVTCT-BALB) did not produce infectious FV, although retrieval of infectious FV occurred when these cells were co-cultivated with cell lines replicating non-defective murine leukemia viruses (MLVs). The level of FV expression in the FVTCT-BALB cell line was studied to understand better the process of FV retrieval. 3H-uridine labelling techniques and reverse transcriptase assays showed that FVTCT-BALB cells did not release C-type virus particles. Nucleic acid hybridization techniques demonstrated that the level of viral RNA synthesis in the FVTCT-BALB non-producer cell line was indistinguishable from that in cell lines productively infected with MLVs. These data suggest that in the FVTCT-BALB cell line the synthesis of FV is blocked in some late stage of virus assembly.
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PMID:Incomplete viral synthesis in Friend leukemia virus-induced reticulum cell sarcomas. 76 87

We have studied synthesis of specific proteins in two permanent lines of Friend virus-induced erythroleukemia cells (Friend line 745 and Ostertag line FSD-1, both derived from DBA/2 mice). By 96 hr following treatment with 1-2% dimethyl sulfoxide (Me2SO), up to 25% of the protein being synthesized by both these cultures is hemoglobin. At that time, hemoglobin constitutes up to 10% of the cellular soluble protein. Both lines synthesize heme and globin coordinately, and alpha and beta globin chains in a nearly balanced 1:1 ratio. However, the ratio of betaMajor:betaMinor chains synthesized by these induced Friend leukemia (FL) cells is approximately 9 in the FSD-1 line and 1.3 in the Friend Clone 745 line, whereas it is 4 in normal adult DBA/2 mouse erythrocytes. Evidence for the latter conclusion was obtained by electrophoresis of FL hemoglobins on cellulose acetate membranes, and also by chromatographic separation of alpha, betaMajor, and betaMinor globins on carboxymethylcellulose in 8 M urea at 20 degrees C. Carbonic anhydrase activity per mg protein is 3 times higher in induced than in control cultures. 2,3-diphosphoglyceric acid is not found in induced FL cells. Induced and control FL cells agglutinate strongly and equally with Phaseolus vulgaris phytohemagglutinin. The developmental process in these cultured leukemia cells appears to be an aberrant erythropoiesis.
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PMID:Synthesis of erythrocyte-specific proteins in cultured friend leukemia cells. 80 34

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.
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PMID:Effect of the nitrosourea derivative rpcnu (ICIG 1163) on the development of Friend leukemia in mice. 89 12

The histopathology of the spontaneous regression of murine leukemia induced by a particular strain of Friend leukemia virus was studied in Swiss ICR/Ha mice. Animals inoculated with the regressing strain of Friend virus exhibited an initial pathologic response identical to that induced by conventional strains of Friend virus. Unlike the fatal leukemia produced by conventional Friend virus, the pathology of the disease induced by the regressing strain of Friend virus appeared to be self-limiting. The histopathology of the two diseases is compared in this report.
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PMID:Histopathology of spontaneous regression in virus-induced murine leukemia. 97 Apr 43

The factors that control oncornavirus formation were analyzed in Friend leukemia cells that undergo hematopoiesis when treated with dimethyl sulfoxide. Suspension cultures of Ostertag FSD-1 cell line were found to enter a G or resting state at the end of their proliferative phase and to simultaneously cease producing helper and dependent components of Friend virus. Whereas the decline in virus production is at least 100-fold, rates of cellular RNA and protein synthesis are only slightly lower in resting than in growing cells. Both resting and growing cells contain similarly large concentrations of the viral proteins P(30) and P(12). Dimethyl sulfoxide induces hemoglobin synthesis in growing cells, but its effects on virus production appear to be indirect results of its action to inhibit cell growth and thus to delay entry of cells into the G resting state. Furthermore, variant cell lines were obtained with differing abilities to synthesize virus or hemoglobin. Some lines no longer produce infectious virus, although they all harbor murine leukemia virus genes which are expressed to varying extents. The major internal protein of these oncornaviruses, P(30), is synthesized in large amounts by all of the cell lines. These results suggest that Friend virus production is not coinduced with erythroid differentiation, as had been proposed, but rather is controlled by a cellular growth cycle.
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PMID:Relationship of Friend murine leukemia virus production to growth and hemoglobin synthesis in cultured erythroleukemia cells. 106 78

Host restriction of exogenous infection by murine leukemia viruses is controlled in vitro predominantly by the murine Fv-1 locus. The mechanism of this host restriction was investigated by comparing the early events in the replication of N-tropic versus B-tropic Friend leukemia virus in NIH 3T3 cells. These cells, which are Fv-1nn in type, are permissive for the N-tropic strain, but nonpermissive for the B-tropic strain, which replicates permissively in Balb/c cells. We have studied the synthesis, intracellular location, and molecular form of virus-specific DNA early in replication by means of molecular hybridization with a virus-specific DNA probe. Our results suggest that in the permissive infection viral DNA rapidly becomes integrated with cellular DNA. However, in the nonpermissive infection, although almost equal amounts of both positive and negative strand viral DNA are synthesized, integration of the provirus does not occur.
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PMID:Host restriction of Friend leukemia virus: synthesis and integration of the provirus. 106 86

Friend virus infection of susceptible mice led rapidly to fulminant erythroleukemia and death. Subcutaneous implantation of leukemia spleen bits into splenectomized normal animals led to their early death from Friend leukemia. In contrast, bits of leukemic spleen implanted sc into splenectomized leukemic mice prolonged the survival of these animals. Concomitant with this survival was a reversal of the virus-induced immunosuppression and an increase in the levels of circulating, neutralizing, antivirus activity. This marked difference in response to leukemic spleen implants by leukemic as compared to normal mice reflected previous contact of the former with Friend Virus. Our studies indicated that the Friend virus-infected mouse mounted a resistance to the virus infection, which under certain conditions is capable of reversing the disease process.
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PMID:The spleen in Friend leukemia. I. Prolonged survival of leukemic mice after autoimplantation of spleen tissue. 106 38


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