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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DNA synthesis was studied in mouse ascites sarcoma cells using a permeable cell system. The sarcoma was induced by the Schmidt-Ruppin strain of Rous sarcoma virus. The cells were made permeable to nucleoside triphosphates by treatment with a hypotonic buffer containing 10 mM Tris Cl, 4 mM MgCl2, 1 mM EDTA, and 6 mM 2-mercaptoethanol (pH 8.0). DNA-synthetic activity in the permeable cells was highly dependent on four deoxyribonucleoside triphosphates, adenosine triphosphates, Mg2+, and a proper ionic environment. The activity was stimulated about 50% by the addition of an appropriate concentration of cytidine triphosphate, guanosine triphosphate, and uridine triphosphate in an assay mixture containing adenosine triphosphate and four deoxyribonucleoside triphosphates. DNA synthesis was confined to the nucleus and was sensitive to N-ethylmaleimide and DNase. The activity assayed by the permeable cell system correlated closely with the DNA-replicating activity assayed by [3H]deoxythymidine incorporation in intact cells. The close correlation between DNA synthesis in vitro and in vivo was further confirmed in cultured sarcoma cells synchronized with DNA synthesis. Analysis of the DNA synthesized in vitro by alkaline cesium sulfate density gradient centrifugation showed that over half the DNA synthesized in permeable cells was due to elongation of strands initiated in vivo. The permeable cell system appears to be a useful method for examining DNA replication of cells in suspensions.
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PMID:DNA synthesis inpermeable mouse ascites sarcoma cells. 18 30

A glucose binding fraction was obtained by sucrose gradient centrifugation and Sephadex G-200 chromatopgraphy from confluent normal cells and Rous sarcoma virus-transformed fibroblasts. It was more or less loosely bound to the membrane fraction, most strongly in sarcoma cells, and most loosely in slowly growing confluent fibroblasts. In an average of three determinations, the content of binding factor was increased 2.5-fold in transformed cells, and compared reasonably well to a nearly 4-fold increase in glucose uptake. The addition of 5 mug/ml of purified glucose binding factor to the overlaying fluid in the 100-mm plates increased 7-flod the low glucose uptake of starved fibroblasts. The stimulation was an additive increment to the known stimulation by calf serum.
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PMID:Isolation from normal and Rous sarcoma virus-transformed chicken fibroblasts of a factor that binds glucose and stimulates its transport. 18 3

Some animal viruses that contain RNA replicate through a DNA intermediate. The molecular details of the replication of these viruses, which are called ribodenoxyviruses, are starting to be known. The ribodenoxyviruses belonging to a single species may either cause sarcomas, leukemia or no disease. The viruses belonging to a single species differ only in whether or not they contain genes for disease formation. In the case of Rous sarcoma virus, the virus causes sarcomas by adding a gene for sarcoma formation to the genome of infected cells. Ribodeoxyviruses appear to undergo different kinds of genetic changes at extraordinarily high rates. In addition, nucleotide sequences related to ribodeoxyvirus RNA are present in the DNA of many uninfected cells. These nucleotide sequences may represent a virus precursor, and ribodeoxyviruses are hypothesized to have evolved from these nucleotide sequences in uninfected cells. These data have led us to hypothesis that non-viral carcinogens act to mutate a cellular gene(s) that is involved in the same types of information transfer and genetic variation as ribodeoxyviruses and thus give rise to the formation of cancer gene(s).
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PMID:RNA viruses and cancer: Lucy Wortham James Lecture (Basic Science). 18 91

Leukosis viruses of seven subgroups were tested for oncogenicity in chickens susceptible to virus infection and to development of lymphoid leukosis (LL) tumors. All subgroup A viruses and the subgroup B virus tested produced a high incidence of LL and other related neoplasms. Viruses of subgroup C and RAV-61 of subgroup F produced a low level of LL. The RAV-50 of subgroup D produced osteopetrosis. In these tests, the viruses of subgroup E and G and one virus of subgroup F were not pathogenic, possibly because infection was not established in the chickens, the chickens were not susceptible to tumor development by these viruses, or the viruses lacked oncogenicity. All temperature-sensitive mutants of Rous sarcoma virus produced sarcomas, but the level varied. One nontransforming mutant produced sarcomas, and the other three tested produced LL. All three mutants that cause cells to grow as colonies in agar produced a high incidence of sarcomas. Thus, sarcoma viruses, by back-mutation, may lose the ability to transform cells in vitro, to make cells grow in agar colonies, or to induce sarcomas in vivo, yet they retain the ability to produce LL. Conversely, it was previously shown that leukosis viruses may be changed into viruses that transform cells in vitro and produce sarcomas in vivo by suitable passage in chicks.
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PMID:Oncogenicity of avian leukosis viruses of different subgroups and of mutants of sarcoma viruses. 19

Electron microscopic heteroduplex analysis of avian RNA tumor viruses has been undertaken by using 35S viral RNA and long, complementary DNA synthesized in vitro. In this initial study, heteroduplex molecules were formed between complementary DNA from Rous sarcoma virus [Prague B strain (Pr-B)] and RNAs from Pr-B and Rous sarcoma virus [Prague C strain (Pr-C)] and from their transformation defective (td) derivatives, td-Pr-B and td-Pr-C. In the case of heteroduplexes with the td viruses, a deletion loop was observed of the order of two kilobases in size and less than one kilobase from the 3' terminus of the RNA. This deletion probably spans part or all of the sequences of one or more genes in the nondefective sarcoma virus which are essential for cell transformation. The sizes and the positions of the deletions in the td-Pr-B and td-Pr-C viruses were slightly, but significantly, different. No nonhomology features were observed in the Pr-B-Pr-C hybrids, thus confirming the close genetic relatedness of the two viruses. All heteroduplexes contained a proportion of circular and dimer molecules. This observation is a direct demonstration that (-) strand DNA transcription begins at an internal position of the RNA genome, proceeds to the 5' end, reinitiates at the 3' end of the RNA, and copies the remainder of the viral genome. Other implications for models of RNA tumor virus replication are also developed from these data.
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PMID:Heteroduplex analysis of avian RNA tumor viruses. 19 11

Thrombin stimulates cell proliferation in cultures of normal chick embryo fibroblasts but not in cells transformed with Rous sarcoma virus. Analysis of medium conditioned by Rous-sarcoma-virus-transformed cultures demonstrates that these cells do not secrete molecules that can inhibit or inactivate thrombin. The interaction of thrombin with these cells was investigated with enzymatically active 125I-thrombin. The amount of cell-associated 125I-thrombin was found to be three times greater with normal cells than with transformed cells. In both types of cell, greater than 50% of the total cell-associated 125I-thrombin was found as a component that was not dissociated from the cells by trypsin treatment, an observation suggesting that a significant portion was not on the cell surface. The amount of the trypsin-insensitive fraction increases with time up to 12 hr, whereas the trypsin-sensitive fraction is saturated after 1-4 hr. Autoradiography of thin sections of 125I-thrombin-treated cells observed by electron microscopy reveals that after 10 hr incubation greater than 70% of the label is localized in the cytoplasm of both normal and transformed cells. Autoradiograms of sodium dodecyl sulfate/polyacrylamide slab gels demonstrate that 40% of the intracellular label is the size of native thrombin with the remainder in two large fragments of 22,000 and 19,500 daltons.
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PMID:Binding and internalization of thrombin by normal and transformed chick cells. 19 17

Superinfection of chicken embryo fibroblasts transformed by the defective Bryan strain of Rous sarcoma virus (BH-RSV) with two different reticuloendotheliosis viruses (REVs), REV strain T (REV-T) or spleen necrosis virus (SNV), resulted in the production of infectious sarcoma virus pseudotypes. These pseudotypes were neutralized by antiserum prepared against SNV and were unable to infect chicken cells preinfected with either REV-T or SNV. These results suggest that defective BH-RSV is able to use the glycoprotein from REV to form infectious pseudotypes. On the other hand, neither REV-T nor SNV was able to supply a functional reverse transcriptase to the polymerase-negative mutant BH-RSValpha, nor was REV-T or SNV able to complement the defect in the internal protein gene of the temperature-sensitive avian sarcoma virus mutant NY45.
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PMID:Formation of reticuloendotheliosis virus pseudotypes of Rous sarcoma virus. 19 82

Recombination between viral and cellular genes can give rise to new strains of retroviruses. For example, Rous-associated virus 61 (RAV-61) is a recombinant between the Bryan high-titer strain of Rous sarcoma virus (RSV) and normal pheasant DNA. Nucleic acid hybridization techniques were used to study the genome of RAV-61 and another RAV with subgroup F specificity (RAV-F) obtained by passage of RSV-RAV-0 in cells from a ring-necked pheasant embryo. The nucleotide sequences acquired by these two independent isolates of RAV-F that were not shared with the parental virus comprised 20 to 25% of the RAV-F genomes and were indistinguishable by nucleic acid hybridization. (In addition, RAV-F genomes had another set of nucleotide sequences that were homologous to some pheasant nucleotide sequences and also were present in the parental viruses.) A specific complementary DNA, containing only nucleotide sequences complementary to those acquired by RAV-61 through recombination, was prepared. These nucleotide sequences were pheasant derived and were not present in the genomes of reticuloendotheliosis viruses, pheasant viruses, and avian leukosis-sarcoma viruses of subgroups A, B, C, D, and E. They were partially endogenous, however, to avian DNA other than pheasant. The fraction of these nucleotide sequences present in other avian DNAs generally paralleled the genetic relatedness of these avian species to pheasants. However, there was a high degree of homology between these pheasant nucleotide sequences and related nucleotide sequences in the DNA of normal chickens as indicated by the identical melting profiles of the respective hybrids.
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PMID:Nucleotide sequences derived from pheasant DNA in the genome of recombinant avian leukosis viruses with subgroup F specificity. 19 37

Transformation-defective (td) mutants of the Schmidt-Ruppin strain of Rous sarcoma virus (RSV), which contains deletions in the gene responsible for transformation (src gene), are unable to transform chicken embryo fibroblasts in vitro. Injection of some of these td mutants into newborn chickens resulted in the formation of sarcomas from which sarcoma virus was unfailingly recovered. The possibility that transforming RSV was present in the td virus preparations was excluded by further purification of the td viruses. Morphology of the foci induced by the newly recovered sarcoma virus was distinct from that of foci induced by the parental Schmidt Ruppin strain of RSV. It is suggested that the new sarcoma virus was generated as a result of the genetic interaction between the genomes of td virus and chicken cells.
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PMID:Recovery of avian sarcoma virus from tumors induced by transformation-defective mutants. 20 Jul

The genome size of 20 transformation-defective (td) viruses derived from different strains of Rous sarcoma viruses [Prague (subgroups A and C), Schmidt-Ruppin (subgroups A and D) (SR-D), Bratislava 77, and Carr-Zilber subgroup D)] was examined by polyacrylamide gel electrophoresis. All of the td viruses except td SR-D have 35S RNA of the same size-i.e., class b RNA. Two of five td SR-D viruses examined have a slightly larger RNA, corresponding to a td deletion that is about 25% smaller than that of class b RNA. However, the RNase T(1)-oligonucleotide fingerprints of all the td SR-D viruses are identical, lacking two sarcoma-specific oligonucleotides. The fingerprints of these viruses also showed a minor oligonucleotide present at very low concentration. A study of heteroduplex molecules formed between genome-length cDNA made from wild-type SR-D and 35S RNA of td SR-D showed a deletion loop of 2.0 and 1.5 kilobases, respectively, at the map position of the src gene for these two classes of td SR-D viruses, confirming the results of polyacrylamide gel electrophoresis. In addition, some heteroduplex molecules with a substitution loop of 0.6-0.7 kilobase at the same site as the deletion loop were observed in all five of the td SR-D viruses. We conclude that some of the td SR-D viruses have a partially deleted src gene and that all of the td SR-D viruses have incorporated heterologous sequences of distinct length in some RNA molecules at the position of the src gene. The nature and origin of these heterologous sequences are discussed.
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PMID:Occurrence of partial deletion and substitution of the src gene in the RNA genome of avian sarcoma virus. 20 Sep 31


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