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)

The env gene of a bovine leukemia virus (BLV) tumor-derived proviral DNA clone has been located by comparison of the translated DNA sequence with amino acid sequence data on purified gp60 and p30env (A. M. Schultz, T. D. Copeland, and S. Oroszlan (1984) Virology 135, 417-427). There is a continuous open reading frame from the N terminus of gp60 for 1446 nucleotides; gp60 is predicted to contain 268 amino acids and p30env, 214. The predicted p30env shows structural features typical of type C viral transmembrane proteins. It is also clearly related to that of the human T-cell leukemia virus (HTLV), as predicted from the DNA sequence of Seiki et al. (M. Seiki, S. Hattori, Y. Hirayama, and M. Yoshida (1983) Proc. Natl. Acad. Sci. USA 80, 3618-3622) The two proteins show 36% identities in their amino acid sequence, in an alignment requiring six gaps. More distant relatedness is also seen between BLV p30env and both murine leukemia virus p15E and Rous sarcoma virus gp36. The gp60s of BLV and HTLV are more distantly related than their p30envs, but their homology is nonetheless statistically significant. Between the presumptive terminator of the env gene and the beginning of the 3'-long terminal repeat is a region of 1817 base pairs of unknown function. Just as in the HTLV post-envelope sequence, there are at least two reading frames which are open for a significant fraction of this region. In neither the tumor-derived clone nor a clone from a virus-producing cell line, however, is there a continuous open reading frame throughout the region. Comparison of the BLV and HTLV sequences within the post-envelope region revealed a very limited but possibly significant similarity.
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PMID:The nucleotide sequence of the env gene and post-env region of bovine leukemia virus. 609 63

A molecular recombinant of Rous sarcoma virus and murine amphotropic leukaemia virus, src(MoMuLV), where the avian src oncogene has been placed under the influence of a murine virus promoter sequence, has been reported. Infection of long-term marrow cultures with this virus led to a dramatic change in the relative numbers of stem cells, granulocyte-macrophage progenitor cells and mature cells found in normal haematopoietic cell development. However, although the balance between self-renewal, differentiation and development was disturbed, injection of the cultured cells into irradiated syngeneic recipients did not lead to the development of leukaemia. Thus, although the control had been 'loosened', the host regulatory mechanisms were sufficient to impose a restraint on unlimited growth of the cells. We now show that the stem cells from the src-infected cultures show a remarkably increased capacity for self-renewal in vitro in situations which are inimical to the maintenance of self-renewal in normal uninfected stem cells and that self-renewal/differentiation can be modified by the culture conditions.
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PMID:Continuous in vitro generation of multipotential stem cell clones from src-infected cultures. 614 32

A new heterologous system of radioimmunoassay (p24 of bovine leukemia virus--antiserum to Rous sarcoma virus) has been developed which demonstrated for the first time the existence of a common antigenic determinant in the major inner protein of unrelated oncoviruses: avian leukemia-sarcoma virus, bovine leukemia virus, mammalian type C viruses (mouse, hamster, monkey) and type D viruses (simian Mason-Pfizer virus). These data suggest a common origin of unrelated oncoviruses and open new approaches for the search of unknown agents associated with human and animal neoplastic diseases.
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PMID:[Detection of a common antigenic determinant in the major inner protein of unrelated oncoviruses]. 615 38

The nucleotide sequences encoding the transforming polyproteins of the Snyder-Theilen and Gardner-Arnstein strains of feline sarcoma virus (FeSV) have been determined. These sequences include a viral transforming gene (v-fes), derived from cellular proto-oncogene sequences (c-fes) of domestic cats by recombination with feline leukemia virus (FeLV). The v-fes sequences are predicted to encode a polypeptide domain strikingly similar to that specified by the transforming gene (v-fps) of the avian Fujinami sarcoma virus. In addition, the 3' 0.8 kilobase pairs of v-fes encode amino acid sequences homologous to the carboxy-terminal portion of pp60src, the transforming protein encoded by the avian Rous sarcoma virus src gene. Thus different feline and avian retroviral transforming genes, all of which encode functionally related proteins with associated tyrosine-specific kinase activities, must be derived from divergent members of the same proto-oncogene family.
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PMID:Nucleotide sequences of feline retroviral oncogenes (v-fes) provide evidence for a family of tyrosine-specific protein kinase genes. 618 5

Avian retroviruses of subgroups B and D efficiently infect chicken (C/E) but not turkey (T/BD) cells. We describe here three variants of subgroup B and D viruses that infect both cell types equally well. One of these viruses, NTRE-4, was a recombinant between transformation-defective Prague (Pr) strain Rous sarcoma virus (RSV) subgroup B and the endogenous virus RAV-0; the second, SR-DE-1, was a recombinant between Schmidt-Ruppin RSV subgroup D and defective endogenous virus information. T1 oligonucleotide fingerprint analysis of the genomes of these two viruses showed only a small alteration in the portion of the env gene responsible for subgroup specificity, as indicated by the presence of a single subgroup E oligonucleotide in an otherwise purely subgroup B or D gene. The third virus, hrBO1Pr-B, was a variant of Pr-RSV-B that did not appear to be a recombinant and whose altered host range we attribute to mutation. Analysis of the host range of all three viruses by infection of selectively resistant cells and by interference testing indicates that all use the subgroup B receptor on chicken cells and the subgroup E receptor on turkey cells. These viruses may be analogous to the polytropic recombinant viruses recently found to be associated with leukemia in some strains of mice.
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PMID:Mutant and recombinant avian retroviruses with extended host range. 624 65

Contamination of Japanese quail, strain Pharaoh, cell culture with oncogenous and infectious avian viruses was studied. The susceptibility of the embryonal cell cultures of the Japanese quail, strain Pharaoh, to measles, parotitis and fixed rabies viruses was also determined. It was found that the sera of pubertal quails had no antibody to Rous sarcoma virus (RSV), strains Brian, RSV (RAV-1), Schmidt-Ruppin, Carr-Zilber, as well as to Marek's disease and Newcastle disease viruses. No reverse transcriptase activity was detected in the embryonal alantoic fluid of this avian species. The quails were less susceptible, as compared to the chicken, to Schmidt-Ruppin and Carr-Zilber strains of RSV. Measles, parotitis and fixed rabies viruses reproduced actively in the Japanese quail, Pharaoh strain, embryonal cell cultures. It is suggested that the embryonal cell cultures of this avian species can be used as a leukemia-free substrate for experimental studies and manufacturing of viral vaccines.
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PMID:["Pharaoh" line culture of Japanese quail cells as a leukosis-free system for virus reproduction]. 625 36

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

RNA tumor virus-transformed cell cultures derived from rat, mouse, hamster, and mink were examined for their response to cytochalasin B (CB), and the expression of this marker was correlated with growth in soft agar and tumorigenicity in vivo. Continuous cell lines transformed and chronically infected with Moloney murine sarcoma-leukemia virus (M-MSV-MuLV) or Kirsten murine sarcoma-leukemia virus were extensively multinucleated when treated with CB. Similarly, nonproducer Moloney murine sarcoma virus- or Rous sarcoma virus-transformed cells multinucleated in response to CB treatment, whereas uninfected or murine leukemia virus-infected cells remained predominately binucleate under comparable conditions. Rat kidney or embryo cell cultures, one to two passages after infection with M-MSV-MuLV, were highly multinucleated following CB treatment and acquired the ability to grow in soft agar. Mouse 3T3 cell lines, newly infected with M-MSV-MuLV, exhibited a moderate degree of CB-induced multinucleation. CB-induced multinucleation was directly correlated with anchorage-independent growth for most of the cell lines tested. An exception was the Moloney murine sarcoma virus-transformed mink cells which multinucleated in response to CB treatment but were unable to proliferate in soft agar. CB-induced multinucleation was directly correlated with the tumorigenicity of M-MSV-MuLV-transformed rat cells in syngeneic animals. These results demonstrate that CB-induced multinucleation is a useful in vitro growth-related marker of cell transformation by RNA tumor viruses and, in addition, show that this parameter of cell transformation is closely correlated with anchorage-independent growth in vitro and tumorigenicity in vivo.
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PMID:Multinucleation in the presence of cytochalasin B by RNA tumor virus-transformed cells. 625 45

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


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