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At least 19 recordsLinked to original sources
PubMed1984

RNA tumor viruses, DNA tumor viruses and developmental switches: a unifying hypothesis.

It is hypothesized that oncogenic viruses (both RNA and DNA tumor viruses) use cellular differentiation switches as part of their mechanism for viral replication. Chemical or radiation-induced carcinogenesis is the result of mutations which also affect these differentiation switches and their cellular controls. A transformed cell is characterized by the uncontrolled and inappropriate expression of embryonic (developmental) sequences. Many of the oncogenic viruses, both RNA and DNA, are lineage- and stage-specific in the cells they can productively infect, in keeping with their means of replication. The interaction between virus and host cellular controls determines whether recognizable neoplasia will result from viral infection.

Animals↗
PubMed2005

Modulation of the ARF-p53 pathway by the small DNA tumor viruses.

The small DNA tumor viruses encode proteins that subvert many of the pivotal growth regulatory pathways within the cell to facilitate their own replication. The cell responds to viral infection/proteins by activating the p53 tumor suppressor pathway. Activation of p53 could impair a productive viral infection at many levels, including the inhibition of viral DNA replication and/or the premature death of infected cells. Therefore, DNA viruses encode proteins that inactivate the p53 tumor suppressor pathway. Understanding how DNA viral proteins activate/inactivate the p53 pathway has provided invaluable insights into tumorigenesis. Recent studies with polyoma virus have identified a viral protein (PyST) that inhibits ARF-mediated activation of p53, and revealed a novel role for PP2A in the regulation of the ARF-p53 tumor suppressor pathway.

ADP-Ribosylation Factor 1↗
PubMed1987

The analysis of Yaba monkey tumor virus DNA.

Yaba monkey tumor virus DNA was analyzed by digestion with the restriction enzymes Hind III, Eco R I, Bam H I, Sal I, and Bgl I. The restriction fragments from 0.7% and 1.4% agarose gels were used to determine an average molecular weight of 95.0 X 10(6). The location of the terminal cross-links was determined using formamide denaturation. Bam H I fragments D and K (molecular weight 9.6 X 10(6) and 3.3 X 10(6), respectively) were shown to be cross-linked.

Animals↗
PubMed1987

Mammary preneoplasia and tumorigenesis in the BALB/c mouse: structure and modification of mouse mammary tumor virus DNA sequences.

Mouse mammary tumor virus (MMTV) DNA sequences were examined in mammary tissues from BALB/c mice, including both preneoplastic hyperplastic alveolar nodule (HAN) outgrowth lines, tumors derived from those preneoplastic tissues, and DMBA-induced mammary tumors. Over 60 different HAN and tumors samples were analyzed. The D2 HAN line contained one additional provirus, whereas Cv-2 and Cv-4 HAN lines that are infected with exogenous virus exhibited multiple virus integration events. D2 tumors showed the same provirus pattern as D2 HANs, whereas Cv-2 and Cv-4 tumors exhibited a subset of the acquired proviruses found in the parental HAN populations. Differential methylation patterns of virus-specific sequences were observed that resembled those described for other tissues in which viral DNA replication and integration has occurred, i.e., acquired proviruses were hypomethylated and endogenous proviruses were methylated. In tumors that arose from HAN lines and exhibited only endogenous proviruses, demethylation of the subgenomic Mtv-6 locus was observed. Demethylation of Mtv-6 was not detected in any of the preneoplastic tissues. Altered methylation of Mtv-8 and -9 was observed in both Cv-2 and Cv-4 tumors. Finally, mammary tumors induced by DMBA carried no acquired proviruses and demethylation of endogenous MMTV proviruses was demonstrated.

5-Methylcytosine↗
PubMed1992

Five DNA tumor viruses undetectable in human retinoblastomas.

Retinoblastoma (RB) is a childhood eye cancer that arises when a retinal cell lacks a functional RB gene. Recent data indicate the transforming proteins of adenovirus, papillomavirus, and the polyomaviruses BK and JC all can bind to the product of the RB gene. Furthermore, adenovirus 12, JC virus, and simian virus 40 are able to induce RB-like tumors in rodents. In view of these findings, 50 human RBs were tested for the presence of five human DNA tumor viruses: adenovirus 12, BK virus, JC virus, and human papillomaviruses 16 and 18. Using the polymerase chain reaction, no viral sequences were detected in 50 RB DNAs. These data provide no evidence that these viruses have an etiologic role in human RB.

Base Sequence↗
PubMed2003

Mechanisms by which DNA tumor virus oncoproteins target the Rb family of pocket proteins.

Small DNA tumor viruses have evolved different mechanisms to abrogate the function of the retinoblastoma tumor suppressor (pRb). Studies of these viruses have been invaluable in uncovering the central role of the Rb family of pocket proteins in cell cycle control. While the molecular mechanisms by which the viral oncoproteins inactivate the Rb family are still being elucidated, it is clear that targeting of this family is required both for viral replication and for virus-induced transformation of mammalian cells. This review compares and contrasts the approaches DNA tumor viruses have evolved to antagonize Rb family members--ranging from relatively simple equilibrium dissociation of pRb from cellular pRb-binding factors to chaperone-mediated alterations in pocket protein stability and phosphorylation levels. The review will focus on the viral oncoproteins adenovirus E1A, human papillomavirus E7 and the large T antigens of several polyomaviruses. An understanding of these mechanisms may provide further insight into the regulation and functions of Rb family members as well as uncover new targets for the development of novel anti-viral agents, particularly against human papillomavirus, which is a significant cause of human cancer.

DNA Tumor Viruses↗
PubMed1987

A novel system for studying in vivo effects of tumor promoters on DNA tumor viruses.

An animal system is described that allows the analysis of the interaction of persisting hamster papovavirus (HaPV) genomes with the tumor-promoting phorbol ester TPA. In a colony of HaPV-bearing Syrian golden hamsters, extrachromosomal HaPV genomes were detected by Southern blot hybridization in DNA isolated from skin biopsies. Chronic topical treatment of hamsters with TPA resulted in a dramatic increase of viral DNA in skin cells at the site of TPA application. After finishing the TPA treatment, the amount of extrachromosomal viral DNA declined but was still enhanced more than three months thereafter. This model offers the possibility of investigating, at the molecular level, the initiating role of virus in tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1973

RNA-DNA covalent bonds between the RNA primers and the DNA products formed by RNA tumor virus DNA polymerase.

Initiation of DNA synthesis by endogenous RNA primer molecules was studied with three different RNA tumor viruses. The influence of the method of virus disruption on the observed RNA-DNA bonds was ascertained. Ether disrupted virions of both murine leukemia virus (MuLV) and the B77 strain of avian sarcoma virus (B77 virus) have rC-dC and rA-dA covalent linkages between RNA primers and newly synthesized DNA. None of the 14 other possible bonds were formed. Ether-disrupted virions of avian myeloblastosis virus (AMV) have rU-dC and rA-dA linkages. In contrast, work reported herein and from other laboratories shows that Nonidet P-40 (NP-40)-disrupted virions of all three viruses have only the rA-dA junction. Studies with virus particles which were first disrupted with ether and then treated with NP-40 indicated that the detergent treatment disallowed the formation of the ribopyrimidine-dC internucleotide bond. The same transfers are found with AMV in the presence or absence of actinomycin D, where only single-stranded DNA is formed. This finding is consistent with the notion that virtually all of the significant primers have been recognized. In contrast to mature virions, transfer experiments with ether-disrupted early harvest (5 min) MuLV showed only the rC-dC bond; the rA-dA bond was absent. The short-time harvest contains a significantly higher proportion of infectious virions than 24-h harvests. Also, since the RNA from early harvest virus is appreciably more homogenous than the RNA of mature MuLV, it is concluded that the ribopyrimidine-dC linkage is the more significant initiation event from a biochemical standpoint.

Alpharetrovirus↗
PubMed1985

Sequence organization and molecular cloning of mouse mammary tumor virus DNA endogenous to C57BL/6 mice.

The sequence organization of mouse mammary tumor virus DNA endogenous to the C57BL/6 inbred mouse strain was characterized by Southern blot analysis, utilizing probes specific for particular regions of the mouse mammary tumor virus provirus and by molecular cloning of endogenous mouse mammary tumor virus DNA. The genome of C57BL/6 mice contains three apparently intact, endogenous proviral units; two of these units comprise the Mtv-8 (unit II) and Mtv-9 (unit III) genetic loci that are also present in the DNA of BALB/c mice. The third unit is defined by EcoRI restriction fragments of 10.0 and 8.4 kilobases that contain the 5' and 3' portions of the provirus, respectively. This unit, termed unit XI and encoded by the genetic locus Mtv-17, has not been previously recognized in C57BL/6 DNA, but it can be clearly distinguished from the proviral units at Mtv-8 and Mtv-9 by Southern blot analysis under appropriate conditions. The proviral unit at Mtv-17 is not present in BALB/c DNA. DNAs comprising the entire Mtv-8 locus and the 3' portions of Mtv-9 and Mtv-17 were cloned. Analysis of the cloned DNA revealed no obvious deletions or rearrangements that would render proviral DNA defective; however, these endogenous genes are normally not transcriptionally active.

Animals↗
PubMed1993

DNA tumor virus transforming proteins and the cell cycle.

Studies using the transforming proteins of the small DNA tumor viruses point to the role of the E2F cellular transcription factor in regulating cell cycle specific gene expression. The evidence derived suggests that E2F is controlled by the retinoblastoma gene product and related proteins, including their associated cyclins. Studies using DNA tumor virus products further suggest the existence of additional pathways of cell-cycle activation.

Amino Acid Sequence↗
PubMed2007

Human retinoblastoma is not caused by known pRb-inactivating human DNA tumor viruses.

Retinoblastomas occur as the consequence of inactivation of the tumor suppressor retinoblastoma protein (pRb), classically upon biallelic inactivation of the RB1 gene locus. Recently, human papillomavirus (HPV) genomic DNA has been detected in retinoblastomas. To investigate the possibility that oncoproteins encoded by pRb-inactivating DNA tumor viruses play a role in the pathogenesis of human retinoblastoma, 40 fresh-frozen tumors were analyzed for the presence of HPV, adenovirus (HAdV) and polyomavirus (BKV, JCV and SV40) genomic DNA sequences by real-time polymerase chain reaction (PCR). Tumors were screened for genetic and epigenetic alterations in all 27 exons of the RB1 gene locus and promoter by exonic copy number detection, sequencing and methylation-specific PCR of the promoter region. Retinoblastoma tumors from children with bilateral familial (n=1), bilateral nonfamilial (n=1) and unilateral nonfamilial (n=38) disease were analyzed. Inactivating modifications to the RB1 gene locus were identified on both the alleles in 27 tumors, one allele in 8, and neither allele in 5 cases. A median of over 107,000 tumor cells were analyzed for viral genomic DNA in each PCR reaction. All tumor samples were negative for 37 HPV types, 51 HAdV types, BKV and JCV genomic sequences. Very low copy number (0.2-260 copies per 100,000 tumor cells) SV40 genomic DNA detected in 8 of 39 samples was demonstrated to be consistent with an artifact of plasmid-derived SV40. In contrast to recent reports, we obtained substantial quantitative evidence indicating that neither HPV nor any other pRb-inactivating human DNA tumor viruses play a role in the development of retinoblastoma, regardless of RB1 genotype.

Child↗
PubMed1996

Large T antigen coding sequences of two DNA tumor viruses, BK and SV40, and nonrandom chromosome changes in two glioblastoma cell lines.

The T antigen (TAg) coding sequences of two DNA tumor viruses, BKV and SV40, were detected by Polymerase Chain Reaction (PCR) amplification followed by Southern-blot hybridization in two human glioblastoma multiforme derived cell lines. RT-PCR analysis indicated that these two TAg coding sequences were expressed in both tumor cell lines carrying the viral early region DNAs. Moreover, analytical polyacrylamide gel electrophoresis (PAGE) and DNA sequence analyses showed that the amplified PCR products are indistinguishable from the TAg coding sequences of BKV and SV40 wildtype strains. Cytogenetic study performed in the two cell lines showed unbalanced changes, mainly gains of chromosomes 3p, 5, 6, 7, and 19 and losses of chromosomes 3, 3q, 16, 9p22-->pter, 18, and 20. Excess of chromosomes 6 and 7 are common to the two cell lines. The putative role of the TAg of the two DNA tumor viruses in transformation and karyotype changes is discussed.

Antigens, Viral, Tumor↗
PubMed1982

Mammary tumor virus DNA as a marker for genotypic variance within hormone-responsive GR mouse mammary tumors.

Mammary tumors of GR mice acquire extra mammary tumor virus (MMTV) DNA information within their DNA during tumor growth and development. These extra MMTV genes have been used by us as genotypic markers to investigate the heterogeneity of GR mammary tumors and their loss of hormone dependence during serial transplantation. Our studies reveal that the various subpopulations of cells within individual GR mammary tumors are characterized by differences in number and location of acquired extra MMTV DNA fragments. Losses of certain of these extra MMTV DNA fragments occur when mammary tumors become hormone independent, indicating a loss of hormone-dependent cells. The study of MMTV DNA markers also reveals that low levels of autonomous cells are already present in some hormone-dependent mammary tumors at an early stage of their development. The genotypic analysis strongly indicates that mammary tumor progression is not due to phenotypic adaptation but to clonal selection of the more aggressive sublines.

Animals↗
PubMed2001

Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus.

Kaposi's sarcoma-associated herpesvirus (KSHV) is a newly identified gammaherpesvirus associated with all clinical forms of Kaposi's sarcoma (KS), body-cavity-based, primary effusion lymphomas (PELs), and a subset of Castleman's disease (CD). Sequence analysis of the KSHV genome demonstrates an extensive array of genes with homology to cellular genes involved in cell cycle regulation, cell proliferation, apoptosis, and immune modulation. Functional studies indicate that these genes may modify the host cell environment, contributing to the pathogenesis of KSHV-associated disorders. Several KSHV genes have been found to cause dysregulated cell proliferation or to interfere with established tumor suppressor pathways. The epidemiologic association of KSHV with malignancies and the coding features of its genome suggest that it is a new DNA tumor virus.

Apoptosis↗
PubMed1982

Carcinogen-transformed human cells are inhibited from entry into S phase by fusion to senescent cells but cells transformed by DNA tumor viruses overcome the inhibition.

Senescent human diploid cells (HDC) were fused to replicative transformed cells of different types, and DNA synthesis was monitored in the resulting heterodikaryons. Human cells transformed by simian virus 40 or adenovirus serotype 5 were able to induce DNA synthesis in senescent HDC nuclei in heterodikaryons. In contrast, carcinogen-transformed cells were not able to induce DNA synthesis in senescent HDC nuclei; rather, the transformed nuclei in these heterodikaryons were inhibited from entering S phase. Cells transformed by Rous sarcoma virus and most human tumor cells tested are similarly inhibited by fusion to senescent HDC. These results suggest that the mechanism for transformation by DNA tumor viruses may be fundamentally different from that of other viruses and carcinogens and from that of most human tumor cells. A simple model to explain these results is that (i) senescent HDC contain an inhibitor of entry into S phase; (ii) cells transformed by DNA tumor viruses have gained a transforming factor, perhaps large tumor antigen, that is capable of overriding the normal inhibitor; and (iii) cells transformed by carcinogens or RNA viruses have lost or altered the mechanism for expression of the normal inhibitor yet are still sensitive to it. We propose that this inhibitor is produced in normal cells when they experience conditions that are inadequate for proliferation and that it plays a role in putting the cells into a distinct quiescent state with long-term viability. The override of this inhibitor function in simian virus 40-transformed HDC can explain why they have low viability in plateau-phase cultures and why they die during crisis.

Carcinogens↗