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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The only known product of the Snyder-Theilen strain of feline sarcoma virus (ST-FeSV) is a 85,000-dalton protein, designated ST P85, that contains feline leukemia virus gag gene encoded proteins (p15, p12, and a fragment of p30) and a sarcoma virus-specific polypeptide. Antibodies directed against the latter immunoprecipitated a 92,000-dalton phosphoprotein (NCP 92) expressed at low levels in normal feline embryo fibroblasts as well as in feline cells of epithelial or lymphoid origin. Normal cellular proteins crossreactive with ST P85 were also detected in cell lines from various other mammalian species. These results suggest that the ST-FeSV sequences encoding for the sarcoma virus-specific domain of ST P85 originated from an evolutionarily conserved cellular gene expressed in cells of independent differentiation lineage. Immunoprecipitates containing ST-FeSV P85 exhibited a protein kinase activity that specifically phosphorylated tyrosine residues. The physiological significance of this finding is illustrated by the finding that phosphotyrosine is an intrinsic component of ST P85. Furthermore, 5- to-fold higher levels of this unusual phosphorylated amino acid were present in ST-FeSV transformants than in uninfected control cells. Phosphorylation of tyrosine residues appears to be associated with cellular transformation caused by Rous sarcoma virus and Abelson murine leukemia virus. Thus, independent transforming virus isolates from birds, mice, and cats may utilize common pathways in exerting their oncogenic potential.
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PMID:Origin and functional properties of the major gene product of the Snyder-Theilen strain of feline sarcoma virus. 625 60

Fujinami sarcoma virus (FSV) of chickens does not contain nucleotide sequences related to the src gene of Rous sarcoma virus, but it carries unique sequences of at least 3000 bases, which are likely to code for the transforming protein of this virus. Using radioactive DNA complementary to FSV-unique sequences, we investigated the relatedness of FSV to other sarcoma-leukemia retroviruses in vertebrates. Under conditions of moderate stringency, no cross-hybridization was detected between FSV cDNA and RNAs of Rous sarcoma virus, Y73 avian sarcoma virus, several representative avian acute leukemia viruses, or Abelson murine leukemia virus. This cDNA, however, did hybridize with RNA of PRCII sarcoma virus of chickens to the extent of 56%. In addition, FSV cDNA was found to hybridize with RNAs of Gardner-Arnstein and Snyder-Theilen strains of feline sarcoma virus to the extent of 27% and 19%, respectively, but not with RNA of McDonough feline sarcoma virus. Studies on thermal denaturation of hybrids showed that the melting temperatures of the heteroduplexes of the FSV cDNA with RNAs of PRCII and Gardner-Arnstein feline sarcoma virus were 7 degrees C and 12 degrees C lower, respectively, compared with the melting temperature of the homologous hybrid of FSV, and suggested less than 10% mismatching in both heteroduplexes. These results indicate that nucleotide sequences closely related to at least a part of FSV-unique sequences are present in the genomes of other sarcoma viruses obtained in chickens and in cats.
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PMID:Homology exists among the transforming sequences of avian and feline sarcoma viruses. 625 42

Type C sarcoma viruses are genetic recombinants containing portions of replication-competent helper viruses linked to sarcoma virus-specific sequences (generically designated onc genes) which are thought to be required for acute fibroblast transformation. The onc elements of different avian and mammalian sarcoma viral isolates are each homologous to subsets of cellular DNA sequences which have no well-defined role in normal cells. Because of the lack of significant homology between helper viral genes and cellular onc sequences, the recombinational mechanisms which facilitate the formation of sarcoma viral genomes remain unclear. In Moloney murine sarcoma virus, viral onc (or v-mos) and cellular onc (or c-mos) sequences exhibit complete and uninterrupted homology as determined by heteroduplex and restriction enzyme analyses of molecularly cloned DNA. By contrast, the cellular counterparts of the onc elements of Rous sarcoma virus (G. Cooper and R. Parker, personal communication), avian erythroblastosis virus (B. Vennstrom, personal communication), Abelson leukaemia virus (D. Baltimore, personal communication), Harvey sarcoma virus (E. Scolnick, personal communication) and simian sarcoma virus (R. Gallo, personal communication) are now known to contain intervening sequences which do not appear in the respective viral genomes. Here we report the use of the Southern blot technique to examine cat cellular DNA sequences (c-fes) homologous to the onc gene (v-fes) of Snyder-Theilen feline sarcoma virus (ST-FeSV). We used cloned DNA 'probes' containing defined portions of the ST-FeSV genome to show that v-fes sequences originate from at least four noncontiguous sequences in cat cellular DNA, separated from each other by intervening sequences.
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PMID:onc sequences (v-fes) of Snyder-Theilen feline sarcoma virus are derived from noncontiguous regions of a cat cellular gene (c-fes). 625 36

The genome of the Snyder-Theilen strain of feline sarcoma virus (ST-FeSV) is a 4.3-kilobase-pair (kbp) RNA molecule that contains a 1.5-kbp cellular insertion (fes gene) flanked by feline leukemia virus sequences at its 5' end (1.6 kbp) and 3' end (1.2 kbp) (Sherr et al., J. Virol. 34:200-212, 1980). DNA transfection techniques have been utilized to determine the regions of the ST-FeSV genome involved in malignant transformation. I have found that the 3.7-kbp 5'-end fragment of the ST-FeSV provirus (which corresponds to the 3.4-kbp 5'-end fragment of the viral genome) is sufficient to transform NIH/3T3 fibroblasts. Enzymes that cleave the ST-FeSV provirus DNA within the feline leukemia virus gag gene sequences or within the fes gene abolished the transforming activity. Preservation of the proviral large terminal repeats was also required for transformation. Transformed NIH/3T3 cells obtained by transfection of total or subgenomic ST-FeSV DNA expressed normal levels of the ST-FeSV gene product ST P85 and of its associated protein kinase activity. Furthermore, these cells contained high levels of phosphotyrosine residues, a biochemical marker associated with cellular transformation induced by certain retroviruses including ST-FeSV. These results, taken together, strongly support the concept that only those ST-FeSV proviral sequences necessary for ST P85 expression are involved in malignant transformation.
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PMID:Cellular transformation by subgenomic feline sarcoma virus DNA. 626 Oct

RNA from the Snyder-Theilen feline sarcoma-leukaemia virus complex (ST-FeSV-FeLV) sedimented in a double-peaked band between 50 and 70S, but Gardner-Arnstein (GA) FeSV-FeLV RNA sedimented in a single 70S peak. FeLV isolated from the ST virus mixture contained RNA which sedimented in a 70S band like GA-FeSV-FeLV RNA, but F422 FeLV RNA sedimented more slowly, at 50 to 60S. After thermal denaturation, resedimentation revealed three classes of RNA subunits in ST-FeSV-FeLV RNA: the first class, 35 to 37S, was also found in ST-FeLV and other FeLVs (except F422 FeLV), in the endogenous feline virus, RD114 and in GA-FeSV-FeLV; the second class, 32 to 34S, was similar to subunits in F422 FeLV and minor components of GA-FeSV-FeLV and ST-FeLV; the third class, 25S, was detected only in ST-FeSV-FeLV RNA. Electrophoresis of RNA species in buffered formamide provided evidence that the three classes of RNA subunits distinguishable on the basis of sedimentation rates actually represent three size classes of subunits. The ST virus mixture was shown to contain about equal titres of infectious FeLV and transforming FeSV whereas GA-FeSV-FeLV had at least a 10-fold excess fo FeLV over FeSV. These observations are discussed in terms of possible origins of the three sizes of FeSV-FeLV RNA subunits and their relationships to three species of FeSV-FeLV proviral DNA described recently (Sherr et al. 1979).
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PMID:Three sizes of subunits in RNAs from feline sarcoma-leukaemia virus mixtures. 626 39

Transformation of chicken cells by Fujinami sarcoma virus (FSV), PRC II or Y73 (three independently isolated avian sarcoma viruses that are replication-defective and lack the Rous sarcoma virus src gene) resulted in significant elevation (4-13 fold) of phosphotyrosine levels in cellular protein. The gag-related proteins encoded by these avian sarcoma viruses (ASVs) were all associated with tyrosine-specific protein kinase activity when assayed in immune complexes and were phosphorylated at both tyrosine and serine residues in vivo. Both the phosphotyrosine level in protein of FSV-infected cells and the protein kinase activity assayed in immune complexes containing the FSV protein P140 were temperature-sensitive. The presumed transforming proteins of these ASVs were compared with those of Rous sarcoma virus (RSV), Abelson murine leukemia virus and the Snyder-Theilen and Gardner-Arnstein strains of feline sarcoma virus (FeSV), which have previously been associated with tyrosine-specific protein kinase activity. FSV and PRC II proteins were shown to be structurally related to one another and to the FeSV proteins by tryptic peptide mapping and by immunological studies. No homology was observed, however, between the transforming proteins of RSV, Y73, Abelson murine leukemia virus and the FSV/PRC II/FeSV class, suggesting there may be at least four classes of retroviruses whose transformation mechanisms involve aberrant phosphorylation of cellular protein at tyrosine residues.
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PMID:Transforming proteins of some feline and avian sarcoma viruses are related structurally and functionally. 626 83

Murine fibroblasts transformed by transfection with DNA from mink cells infected with the Snyder-Theilen strain of feline sarcoma virus and subgroup B feline leukemia virus were analyzed for the presence of integrated proviral DNA and the expression of feline leukemia virus- and feline sarcoma virus-specific proteins. The transformed murine cells harbored at least one intact feline sarcoma virus provirus, but did not contain feline leukemia virus provirus. The transformed murine cells expressed an 85,000-dalton protein that was precipitated by antisera directed against feline leukemia virus p12, p15, and p30 proteins. No feline oncornavirus-associated cell membrane antigen reactivity was detected on the surfaces of the transformed murine cells by indirect membrane immunofluorescence techniques. The 85,000-dalton feline sarcoma virus-specific protein was also found in feline cells transformed by transfection. However, these cells also contained env gene products. The results of this study demonstrate that the feline sarcoma virus genome is sufficient to transform murine cells and that expression of the 85,000-dalton gag-x protein is associated with transformation of both murine and feline cells transformed by transfection.
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PMID:Biochemical characterization of cells transformed via transfection by feline sarcoma virus proviral DNA. 626 44

The successful application of an improved enzyme-linked immunosorbent assay (ELISA) to the specific detection and quantitation of feline leukemia virus (FeLV) is presented. The methods described can detect FeLV antigens at the picogram/milliliter level using a fluorometric assay for peroxidase-linked antibody. The use of a fluorogenic substrate resulted in at least a 9-fold increase in sensitivity of the peroxidase assay. FeLV antigens could be specifically detected in chronically infected cells as well as in feline sarcoma virus-transformed nonproducer mink cells which only partially express viral proteins.
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PMID:Evaluation of the parameters of the ELISA procedure for feline type C retroviral antigens: assay of FeLV antigens in chronically infected or nonproducer transformed cells. 626 65

We isolated a strain of normal goat fibroblasts which was uniquely selective in that it allowed the replication of xenotropic murine leukemia virus but not polytropic recombinant murine leukemia virus. In addition, feline leukemia virus type A replication was severely diminished in these goat cells, whereas feline leukemia virus type B and feline endogenous RD114-CCC viruses replicated efficiently. No other known cells exhibit this pattern of virus growth restriction. These goat cells allow the study of xenotropic murine leukemia virus in mixtures which also contain recombinant murine leukemia virus and may be helpful in eliminating feline leukemia virus type which often coexists in feline sarcoma or leukemia virus mixtures with other feline leukemia virus types.
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PMID:Selective host range restriction of goat cells for recombinant murine leukemia virus and feline leukemia virus type A. 627 Mar 64

The integrated DNA provirus of the Gardner-Arnstein (GA) strain of feline sarcoma virus (FeSV) was molecularly cloned in a bacteriophage lambda vector. The cloned DNA fragment is 14.4 kilobase pairs long and contains a 6.7-kilobase provirus flanked by cellular sequences derived from nonproductively transformed mink cells. Transfection of mouse NIH/3T3 cells with the cloned DNA fragment induced foci of transformation at efficiencies of 10(4) focus-forming units/pmol of sarcoma virus DNA. Restriction endonuclease mapping and heteroduplex analyses were used to compare the GA-FeSV provirus with that of Snyder-Theilen (ST)-FeSV, a second strain that contains homologous transformation-specific sequences (v-fes). Both viruses have the general structure 5'-gag-fes-env-c region-3', each having retained portions of the feline leukemia virus (FeLV) gag and env genes. In addition to segments shared by the two sarcoma viruses, GA-FeSV contains 1.7 kilobases of extra sequences not found in ST-FeSV. Of these, at least 400-500 base pairs located near the 5' end of v-fes encode a portion of the GA-FeSV polyprotein; the remaining 1.2 kilobases are derived from the FeLV env gene but do not appear to encode any detectable product related to the FeLV envelope glycoprotein. The close homology of the v-fes sequences shows that GA- and ST-FeSV were formed by recombination of FeLV with similar portions of a cat cellular gene (c-fes).
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PMID:Recombinant bacteriophages containing the integrated transforming provirus of Gardner--Arnstein feline sarcoma virus. 627 Jun 55


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