DNA Complementary to Viral RNA in Leukemic Cells Induced by Avian Myeloblastosis Virus

Baluda, M A; Nayak, D P

doi:10.1073/pnas.66.2.329

Cited by 74 publications

(58 citation statements)

References 29 publications

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“…1. The specificity of the DNA-RNA hybridization reaction, already documented in previous publications (1)(2)(3)(4) Fig. 2, there is no apparent loss of DNA-RNA hybrids from the filter.…”

mentioning

confidence: 48%

“…As demonstrated (1,4,11,14), the DNA-RNA hybrids formed consist always of long nucleotide sequences, and the average nucleotide composition of the RNA eluted from the hybrids formed with DNA from some normal chicken embryos is nearly identical to that of the input AMV-RNA (11). The best direct evidence, so far, that indicates that viral DNA represents complete or partial DNA copies of ALV genomes, is the acquisition of 3.4 viral DNA equivalents by rat embryonic cells infected with B-77 avian sarcoma virus.…”

Section: Discussionmentioning

confidence: 99%

“…in 3). Previous findings from this laboratory have established that viral DNA complementary to RNA from avian myeloblastosis virus (AMV) was present not only in cells transformed by ALV but also, to a smaller extent, in DNA preparations from pooled, apparently normal, chicken embryos (1,3,4). The specificity of the hybridization procedure and the nature of the DNA-RNA hybrids formed exclude the possibility that the hybrids result from short, accidentally similar, nucleotide sequences of the two nucleic acids.…”

mentioning

confidence: 99%

“…The RNA genome of avian leukosis viruses (ALV) appears to be replicated through a DNA intermediate (1)(2)(3)(4)(5)(6)(7), see also refs. in 3).…”

mentioning

confidence: 99%

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Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Baluda¹

1972

Proc. Natl. Acad. Sci. U.S.A.

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139

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“…1. The specificity of the DNA-RNA hybridization reaction, already documented in previous publications (1)(2)(3)(4) Fig. 2, there is no apparent loss of DNA-RNA hybrids from the filter.…”

mentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

“…The RNA genome of avian leukosis viruses (ALV) appears to be replicated through a DNA intermediate (1)(2)(3)(4)(5)(6)(7), see also refs. in 3).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Baluda¹

1972

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

139

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“…As emphasized by the results of nucleic acid hybridization experiments, it appears clear that some portion (or all) of the viral RNA exists also in DNA form (29)(30)(31)(32)(33)(34)(35). Recently, strong evidence has been provided that, in fact, chicken, mouse, and rat cells contain full viral genomes that can be activated by various treatments (36,39).…”

Section: Discussionmentioning

confidence: 98%

Group-Specific Antigens of RNA Tumor Viruses as Markers for Subinfectious Expression of the RNA Virus Genome

Gilden

Oroszlan

1972

Proc. Natl. Acad. Sci. U.S.A.

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Antigenic markers associated with the major internal protein of RNA tumor viruses of the C-type have proven extremely useful in natural history studies of these viruses. This protein possesses species-specific antigenic determinants, and, in the case of mammalian Ctype viruses, the protein possesses crossreactive determinants as well. These determinants are, thus, useful for species identification and classification of mammalian viruses. A unique distribution of antigens in embryonic tissues of several species (where tests are available) was detected, and in addition, antigen expression in tissues appears to be controlled by a dominant gene. These data have contributed greatly to the theory that RNA tumorvirus information is inherited as part of the cellular genome.

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Viral‐related DNA sequences before and after transformation by RNA tumor viruses

Goodman

Ruprecht

Sweet

et al. 1973

Intl Journal of Cancer

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monkey fibroblasts transformed by non-indigenous R N A tumor viruses ( R S V or FeSV) acquire viral D N A sequences not present in normal cells. The newly gained sequences are always related to those ofthe transforming virus, a result in agreement with the proviral hypothesis. In contrast, the nucleic acid of the indigenous simian RNA tumor virus, SSV-I, exhibits partial homology with the D N A of normal marmoset fibroblasts as well as with SSV-I-transformed cells. Since a similar situation has been observed with avian and lower mammalian systems, it would appear that homology with normal cellular D N A can be used to provide a tool for determining the species of origin of newly isolated R N A tumor viruses.The provirus hypothesis (Temin, 19646) stipulates that infection with a virus must occur to provide the malignant information that ultimately is inserted into the genome of a transformed cell. The prediction is that, after transformation, the DNA will acquire unique sequences not present in normal cells. Conversely, the virogene hypothesis (Huebner and Todaro, 1969;Todaro and Huebner, 1972) suggests that cancer does not normally involve infection with an external virus, but is caused rather by the activation of a viral DNA segment universally present and vertically transmitted in the germ lines of all organisms prone to cancer. Most published investigations of hybridization between viral nucleic acids and cellular DNA nucleic acids have focused on quantitative comparisons before and after viral transformation in homologous systems in which the virus and cells of their natural hosts were used. Some groups (Temin, 1964a; Baluda and Nayak, 1970; Rosenthal et al., 1971; Baluda, 1972) used labelled viral RNA in hybridizations to immobilized DNA and found that infected cells contained more (4-to 6-fold) viral-related DNA than normal cells. However, the normal cells contained more than one viral equivalent per genome and hence no conclusions could be drawn. Others (Wilson and Bauer, 1967; Yoshikawa-Fukada and Ebert, 1969), using the same technique, reported no difference between infected and non-infected cells. This latter conclusion was also derived from hybridizations in solution with vast excess cellular DNA and radioactive viral DNA prepared by endogenous DNA synthesis with disrupted virions (Gelb et al., 1971 ; Varmus et al., 1972a;Varmus et al., 19726 of some viral sequences and the possible absence of others in normal cells. In contrast, in the heterologous system of rat embryo cells transformed by an avian sarcoma virus, 3.4 viral genome equivalents were found per transformed cell, whereas normal rat embryo cells contained at the most 0.1 equivalents (Baluda, 1972). Possibly because it involved the unnatural combination of a chicken virus and a rat cell, this finding was reported without comment at the time. However, because of its potential implications for the oncogenicity of C-type RNA viruses, this observation merited confirmation and extension to other systems.Recently, Varmus et al. (1973) publishe...

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DNA Complementary to Viral RNA in Leukemic Cells Induced by Avian Myeloblastosis Virus

Cited by 74 publications

References 29 publications

Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Group-Specific Antigens of RNA Tumor Viruses as Markers for Subinfectious Expression of the RNA Virus Genome

Viral‐related DNA sequences before and after transformation by RNA tumor viruses

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