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)

A nucleotide sequence was determined for the envelope (env) gene of the polycythemia-inducing strain of the acute leukemia-inducing Friend spleen focus-forming virus (SFFV) and from this the amino acid sequence of its gene product, gp52, was deduced. All major elements of the gene were found to be related to genes of other retroviruses that code for functional glycoproteins. Although the carboxyl terminus of gp52 is encoded by sequences highly related to sequences in its putative parent, ecotropic Friend murine leukemia virus, the majority of the protein (69%), including the amino terminus, is encoded by dualtropic virus-like sequences. Nucleotide sequence comparisons suggest that the nonecotropic region may be more closely related to the 5' substitution in dualtropic mink cell focus-inducing viruses that it is to the 5' end of xenotropic virus env genes. A large deletion and two unique insertions have been located in the env gene of polycythemia-inducing SFFV and may account for some of the unusual structural characteristics, aberrant processing, and pathogenic properties of gp52. As a consequence of the deletion, amino-terminal gp70 and carboxyl-terminal p15E-encoding sequences are juxtaposed and it appears that translation from the p15E region, 3' to the deletion, continues in the standard reading frame used by other retroviruses. Insertions of six base pairs and one base pair at the very 3' end of the gp52-encoding region results in a SFFV-unique amino acid sequence and a premature termination codon.
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PMID:Envelope gene of the Friend spleen focus-forming virus: deletion and insertions in 3' gp70/p15E-encoding region have resulted in unique features in the primary structure of its protein product. 630 46

A Friend mink cell focus-inducing (Fr-MCF) virus isolated from a Friend tumor cell line was able to induce acute erythroleukemia associated with polycythemia when injected as a Friend murine ecotropic leukemia virus (F-MuLV) pseudotype into adult Swiss and ICFW mice. One virus isolate recovered from leukemic cells and designated as FV-F3 presented the following properties: (i) persistence of the same leukemogenic power when propagated in vivo and in vitro; (ii) in vivo spleen focus-forming (SFFV) capacity; (iii) presence of erythropoietin (EPO)-independent CFU-E in leukemic animals; (iv) expression of a 32 RNA specifically recognized by a SFFV probe, in FV-F3 infected cells; and (v) expression in FV-F3-infected cell of polypeptides in the range of gp52 SFFV. Peptide analysis of these products revealed close similarities with the parental MCF virus. These data suggest that a SFFV genome arose by genetic recombinational events involving MCF virus.
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PMID:Genesis of a new spleen focus-forming virus: possible role of MCF viruses. 630 94

A new isolate of a murine erythroblastosis-inducing spleen focus-forming virus (Cas SFFV), derived from the wild mouse ecotropic murine leukemia virus Cas-Br-M, was further characterized after the production of a nonproducer cell line. When rescued from the nonproducer cells with a helper murine leukemia virus, the Cas SFFV induced rapid splenic enlargement and focus formation when inoculated into adult NFS/N mice. The Cas SFFV nonproducer cell line was also utilized to compare the envelope-related glycoprotein of Cas SFFV with gp52s from three strains of Friend SFFV. Cas SFFV was found to encode a 50,500-dalton glycoprotein (gp50) distinct in size to the envelope-related glycoproteins of the Friend SFFVs. The Cas SFFV was also compared in RNA blot hybridization studies. The genomic viral RNA of Cas SFFV was found to be slightly larger than two polycythemia-inducing strains of Friend SFFV and markedly larger than the anemia-inducing strain. Further comparisons between the SFFVs were made by examining their transforming capabilities in an in vitro erythroid burst assay. The erythroid bursts induced by Cas SFFV and the anemia-inducing strain of Friend SFFV showed similarities in their erythropoietin requirements. This study supports our recent observations that Cas SFFV is biologically similar to the anemia-inducing strain of Friend SFFV yet biochemically distinct from all Friend SFFVs.
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PMID:Cas spleen focus-forming virus. II. Further biological and biochemical characterization. 631 69

Stage 1 (pre-malignant) and stage 2 (malignant) cells derived from mice infected with Friend murine leukemia virus or polycythemia-inducing Friend virus complex were examined and compared for the expression of a transformation-related cellular protein, p53. Stage 2 cells were found to express high levels of p53, whereas stage 1 cells did not express detectable levels of this protein. These results indicate that p53 may be a marker for transformed cells present in the second stage of diseases induced by Friend murine leukemia virus or polycythemia-inducing Friend virus complex.
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PMID:Expression of a transformation-related protein (p53) in the malignant stage of Friend virus-induced diseases. 634 27

The levels of serum thymic factor(s) (STF), of Thy-1.2 positivity of splenocytes [as measured by their azathioprine (AZ) sensitivity], and of Thy-1.2-positive "spontaneous" spleen rosette-forming cells (SSRFCs), as well as the presence of infectious virus in the thymus, were assessed as a function of time after virus inoculation in susceptible DBA/2, partially resistant BALB/c, and fully resistant C57BL/6 mice given the polycythemia- or anemia-inducing strain of Friend leukemia virus (FLV-P and FLV-A, respectively). As early as Days 2 to 3, the levels of STF and of AZ sensitivity of splenocytes were profoundly decreased in DBA/2 mice, and, to a lesser extent, in BALB/c mice given FLV-P; however, SSRFCs/spleen were increased in both mouse strains. Conclusive evidence of infectious FLV-P was obtained in the thymuses of DBA/2 mice soon after infection. In mice of the same strains infected with FLV-A, STF levels were similarly decreased, but AZ sensitivity of splenocytes was unaffected, and SSRFCs were decreased. Evidence of early FLV-A infection in the thymus of DBA/2 mice was likewise obtained. In C57BL/6 mice given FLV-A, STF levels, AZ sensitivity of splenocytes, and SSRFC showed changes similar to, but of lower magnitude than, those in BALB/c mice. On the other hand, in C57BL/6 mice given FLV-P, the decrease in STF and AZ sensitivity was almost as pronounced as in susceptible DBA/2 mice in the face of complete absence of infectious virus or viral markers in the thymuses. The observed changes are ascribed to virus infection in view of the following: (a) good temporal correlation between these changes and virus infection; (b) absence of any change in mice given heat-inactivated viruses or spleen homogenate of normal DBA/2 mouse spleen; (c) overall good correlation between mouse genotype and genetic (Fv-1 and Fv-2) restrictions of virus infection on one hand and the magnitude of the observed changes on the other. In particular, the decrease in STF and SSRFC levels is ascribed to the replication-competent (Friend-murine leukemia virus) component of Friend leukemia virus complex, whereas the decrease in AZ sensitivity of splenocytes and the increase of SSRFCs are ascribed to the defective spleen focus-forming virus component of the complex. All changes described so far were transient, since they were not detectable beyond 42 days after virus inoculation in overtly leukemic animals. The observed derangements of thymus-derived immune functions may play an important cofactor role during the onset of leukemia in mice genetically permissive to Friend leukemia virus replication and transformation, but they do not seem relevant to the maintenance of leukemia.
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PMID:Effects of in vivo Friend leukemia virus infection on levels of serum thymic factors and on selected T-cell functions in mice. 634 70

The graft of a transplantable leukemia (IW 32) induced by a biologically cloned helper of a Friend virus devoid of SFFV activity, was shown to induce a polycythemia in recipient animals. An in vitro continuous cell line was derived from this leukemia. The supernatant was shown to induce an erythroid differentiation both in vivo in Mice rendered polycythemic by transfusion, and in vitro in plasma clot CFUE assay. This erythropoietic activity was heat stable (30 min. 56 degrees C, 3 min. 100 degrees C) which ruled out the hypothesis that the IW 32 cell line produced a polycythemia inducing virus. The erythropoietic factor produced by IW 32 leukemic cells might be erythropoietin.
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PMID:[Production of an erythropoietic factor by mouse leukemia]. 641 28

We isolated erythroleukemic cell lines arrested at different levels of the erythroid differentiation pathway. One cell line (CB5), established from mice infected with the helper-independent Friend murine leukemia virus (F-MuLV), exhibited properties similar to those of the normal erythroid progenitor burst-forming cell (BFU-E). Six erythroleukemic cell lines, which were established from the anemia-inducing Friend virus complex (FV-A)-infected mice, formed erythroid colonies similar to the erythroid colony-forming precursor cell (CFU-E) after induction with dimethyl sulfoxide or erythropoietin. Three lines that were established from the polycythemia-inducing Friend virus complex (FV-P)-infected mice also formed low proportions (2-5%) of CFU-E-like colonies after induction by these same inducers. These data, together with the earlier findings that F-MuLV induces an increase in the levels of BFU-E and that FV-A or FV-P stimulates enhancement of CFU-E early after infection, indicate that the erythroleukemic cell lines isolated late in the diseases are at the same levels of differentiation as the leukemic cells in the corresponding initial stages. These cell lines with properties of BFU-E and CFU-E can be induced to differentiate in culture and should add to our understanding of the nature of erythroid progenitor cells and their early differentiation programs.
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PMID:Isolation and induction of erythroleukemic cell lines with properties of erythroid progenitor burst-forming cell (BFU-E) and erythroid precursor cell (CFU-E). 657 10

A transplantable murine leukemia, primarily induced by a biologically cloned Friend helper virus, was shown to induce polycythemia in recipient ICFW mice. A leukemia cell line (IW.32) was established in vitro from this transplantable leukemia. Sodium butyrate and hemin induced erythroid differentiation in these leukemia cells as has already been shown with other erythroleukemia cells. The supernatant of this cell line was devoid of spleen focus-forming virus activity. However, it induced the incorporation of 59Fe in polycythemic mice and the in vitro differentiation of murine and human cfu-e into erythroid colonies. Therefore, these erythroleukemia cells produced a factor with all the biological properties of erythropoietin. The erythropoietic activity of IW.32 supernatant was higher in vitro [equivalent to 0.5-1 international unit (IU) of erythropoietin per ml] than in vivo (0.15-0.3 IU/ml). This erythropoietin-like activity was stable at 100 degrees C for 3 min, which ruled out the possibility that a virus was responsible for these effects. Preliminary studies demonstrated that the biochemical properties of the IW.32 factor are strongly similar to those of Connaught step 3 erythropoietin, thus supporting the hypothesis that the IW.32 factor is indeed an erythropoietin.
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PMID:Production of erythropoietin-like activity by a murine erythroleukemia cell line. 657 7

The concentrations and molecular forms of prealbumin, orosomucoid, albumin, alpha 1-antitrypsin and haptoglobin in leucocytes were studied in patients with alpha 1-antitrypsin deficiency, in acute phase and with leukaemia, by rocket and crossed immunoelectrophoresis. Alpha 1-antitrypsin was the only protein being synthesized by bone marrow cells, blast cells and leucocytes present in the blood during cytotoxic treatment. The other proteins are taken up by the cells. The concentration of alpha 1-antitrypsin in serum and cells was correlated in alpha 1-antitrypsin deficiency and the acute phase, suggesting either that the same signal for synthesis is used in the liver and leucocytes, or that a balance is kept by means of leucocyte uptake. Chronic lymphocytic leukaemia lymphocytes contained only traces of albumin, which may be related to the decreased membrane mobility of these cells. Polycythemia leucocytes, however, contained increased concentrations of all plasma proteins, especially orosomucoid and haptoglobin2 . These two protein forms were found to be markers of mature granulocytes. The cellular concentrations of prealbumin, albumin and transferrin were about 35% of normal in acute myeloid leukaemia cells and no orosomucoid2 and haptoglobin2 was present. Alpha 1-antichymotrypsin was present in a heterogeneous form and the molecular form of alpha 1-antitrypsin (alpha 1 AT4 ) was the same as in monocytes. These findings suggest the existence of a distinct 'AML'-type protein pattern which could be of functional and diagnostic importance.
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PMID:Leucocyte-associated plasma proteins in leucocytes during disease states, and in leukaemic cells. 661 Feb 1

The Friend polycythemia virus complex (FVP), consisting of the replication-defective spleen focus-forming virus (SFFV) and a helper Friend murine leukemia virus (MuLV-F), produces erythroleukemia within 2-3 weeks in vivo. We have recently reported in vitro transformation of bone marrow cells by FVP, producing clusters of erythroid colonies (erythroid bursts) 4-6 days after infection. In contrast to uninfected bone marrow cells, FVP-treated cells proliferated and differentiated (synthesized hemoglobin) in the absence of added erythropoietin, the physiologic regulator of erythropoiesis. The relative roles of helper murine leukemia virus (MuLV) and SFFV in the in vitro erythroid transformation have now been examined. Pseudotype studies and the finding that cloned MuLV-F (free of SFFV) did not induce burst formation indicated that SFFV was essential for this in vitro effect of FVP. Because SFFV could not be obtained free of helper MuLV, we assessed the requirement of MuLV in the transformation by kinetic analyses of helper-deficient and helper-excess FVP preparations. Whereas helper-excess FVP gave single-hit kinetics both in vivo and in vitro, the helper-deficient FVP followed multiple-hit kinetics when titrated for spleen focus formation in vivo. Addition of MuLV-F to helper-deficient FVP prior to injection resulted in a marked enhancement of spleen focus formation and a conversion from multiple-hit to single-hit kinetics. In contrast, titration of this same preparation for erythroid burst transformation in vitro yielded single-hit kinetics, and the addition of helper MuLV-F had no effect. The time course of burst development was similar with or without added MuLV-F. Unlike burst transformation, SFFV production by these infected cultures followed multiple-hit kinetics. Addition of MuLV-F at the time of infection led to an enhancement of SFFV production and conversion of the titration curve from multiple-hit to single-hit. These data are consistent with the idea that SFFV is competent for erythroid transformation in vitro, but requires helper MuLV for its replication.
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PMID:Helper virus is not required for in vitro erythroid transformation of hematopoietic cells by Friend virus. 693 61


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