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At least 19 recordsLinked to original sources
PubMed1985

Evidence for multiple steps in neoplastic transformation of normal and preneoplastic Syrian hamster embryo cells following transfection with Harvey murine sarcoma virus oncogene (v-Ha-ras).

Neoplastic development of Syrian hamster embryo (SHE) cells in culture is a multistep process in which intermediate or preneoplastic cells can be identified and isolated. In an attempt to further characterize normal and preneoplastic cells, we have compared their susceptibilities to neoplastic transformation following transfection with cloned DNA of the oncogenic virus, Harvey murine sarcoma virus (HaMSV). Normal SHE cells, which are stably nontumorigenic when injected in nude mice, are competent to take up and express exogenous DNA as demonstrated by transfection experiments with pSV2-neo DNA and certain viral DNAs. SHE cells treated with 5 micrograms of HaMSV DNA per dish remained nontumorigenic. Colonies of SHE cells, isolated after cotransfection with HaMSV and pSV2-neo DNA and selection for G418 antibiotic resistance, expressed Harvey murine sarcoma virus oncogene (v-Ha-ras) RNA and were initially morphologically altered; however, all colonies senesced when subcultured. In contrast, transfection of the cells with polyoma virus DNA alone or HaMSV DNA plus MC29 viral DNA (pSVv-myc) and then injection of the cells into nude mice resulted in progressively growing tumors of hamster origin within 3 to 5 weeks. A preneoplastic cell line, DES-4, isolated after treatment of SHE cells with the human carcinogen diethylstilbestrol, was chosen for comparative analyses. These immortalized cells are nontumorigenic and excellent recipients for exogenous DNA. In contrast to SHE cells, DES-4 cells were highly susceptible to neoplastic transformation following transfection with HaMSV DNA. To further investigate the role of HaMSV DNA in the neoplastic transformation of DES-4 cells and to determine whether this occurred as a single step, clones of DES-4 cells cotransfected with pSV2-neo and HaMSV DNAs were selected by antibiotic resistance and characterized. There was a good correlation between tumorigenicity and expression of v-Ha-ras DNA; however, the clones were highly variable in terms of their latency periods in vivo and anchorage-independent growth. Neither of these two parameters correlated with the level of expression of v-Ha-ras RNA. All of the cell lines derived from tumors and reinoculated into nude mice had short latency periods in vivo, were highly anchorage independent, and had high levels of v-Ha-ras expression. These results suggest that, in these experiments, v-Ha-ras expression was necessary, but not sufficient, for the tumorigenicity of DES-4 cells and that additional changes in the cells were acquired.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

Interactions between endogenous baboon type-C virus and oncogenic viruses. I. Syncytium induction and development of infectivity assay.

Cells releasing the endogenous baboon virus (BV) can interact with human KC cells containing the Rous sarcoma virus (RSV) genome, resulting in cell fusion and syncytium formation. This interaction has been utilized in the development of a sensitive infectivity assay for BV. The titration pattern is of a one-hit type, demonstrating a linear relationship between virus concentration and number of syncytial plaques obtained in the KC co-cultivation assay. Endpoint titration comparisons indicate that the KC test is as sensitive as the immunofluorescence or the RNA-directed DNA-polymerase assays. Attempts to develop an XC test for BV failed, indicating that while BV can interact with the RSV genome it will do so in the human KC cells and not in the rat XC cells. Syncytia are also induced when KC cells are directly exposed to cell-free BV; however, a linear dose relationship is not obtained. When syncytium-positive KC cultures are passaged, the syncytia disappear and a chronic BV infection is established. These KC-BV cells then lose the ability to interact with either the endogenous cat RD-114 virus or the Mason-Pfizer virus which are known to form syncytia with KC cells.

Animals↗
PubMed1983

[Human oncogenic viruses].

Human oncogenic viruses are ubiquitous pathogens which only in frequently exhibit their malignant potential under natural conditions. They are either ARN viruses, also called retroviruses, of which little is known in man, or DNA viruses belonging to various families (papovavirus, adenovirus, herpes virus, hepatitis B virus), some of which are very specifically associated with certain human carcinomas. In vitro, these viruses induce "cell transformation" producing malignant cells with unregulated growth. In vivo, in man as well as in animals, viral oncogenesis requires multiple cofactors so that the transformed cell can escape control mechanisms.

Animals↗
PubMed2025

Wastewater Sequencing Reveals Persistent Circulation and Rising Prevalence of Several Oncogenic Viruses Across Texas.

BACKGROUND: Oncogenic viruses cause high-risk cancers in humans and are responsible for nearly 20% of all cancer cases worldwide. Currently, very limited data exists in the realm of wastewater-based viral epidemiology (WBE) of cancer-causing viruses, with existing studies using targeted approaches (i.e PCR-based approaches) which lack scalability. Our study aims to carry out WBE with hybrid-capture probes to detect and track multiple oncogenic viruses simultaneously in wastewater across Texas, USA, overcoming the drawbacks associated with targeted approaches. METHODS: Here, we used a hybrid-capture approach to detect, filter and sequence oncogenic virus signals from wastewater samples collected over a duration of three years, from May 2022 to May 2025. Once viral reads were sequenced, we utilized established computational tools to characterize reads into their respective virus of origin. Next, viral abundances of each characterized oncogenic virus were tracked over time and read coverage across their genomes was measured using read mapping techniques. FINDINGS: We detected six known oncogenic viruses, along with three suspected oncogenic viruses across all sampling locations within Texas. Over three years, viral abundance gradually increased, with distinct peaks and dips over the summer and winter months. The prevalence of high-risk viruses such as HPV and EBV rose sharply, with increases in abundance observed post-2024. We also obtained nearly 100% genome coverage with viral reads captured using a hybrid-capture technique for almost all oncogenic viruses and their types. INTERPRETATIONS: Our study shows that a hybrid-capture method can efficiently overcome the challenges faced with using targeted approaches for WBE. Using this method, we get broader read coverage, coupled with concurrent and consistent real-time tracking dynamics of multiple oncogenic viruses. Our findings also emphasize the persistent circulation and rising prevalence of high-risk cancer-causing viruses, underscoring the need for sustained public health interventions to protect communities and assess viral prevalence in high-risk populations. FUNDING: This work was supported by S.B. 1780, 87th Legislature, 2021 Reg. Sess. (Texas 2021), the Baylor College of Medicine and the Alkek Foundation Seed Funds.

Journal Article↗
PubMed1976

Bovine leukemia virus: an exogenous RNA oncogenic virus?

Short term cultures of bovine leukemic lymphocytes release virus particles with biochemical properties of RNA oncogenic viruses. These particles, tentatively called Bovine Leukemia Virus (BLV) have a high molecular weight-reverse transcriptase complex and a density averaging 1.155 g/ml in sucrose solutions. Molecular hybridizations between BLV-3H cDNA and several viral RNAs show that BLV is not related to Mason-Pfizer Monkey Virus (MPMV) Simian Sarcoma Associated Virus (SSV-1) Feline Leukemia Virus (FeLV) or Avian Myeloblastosis Virus (AMV). Rauscher Leukemia Virus (RLV) exhibits a slight but reproducible relatednesse to BLV. The high preference of BLV reverse transcriptase for Mg++ as the divalent cation suggests that BLV might be an atypical mammalian leukemogenic type C virus. Hybridization studies using BLV 3H cDNA as a probe suggest that the DNA of bovine leukemic cells contains viral sequences that cannot be detected in normal bovine DNA.

Animals↗
PubMed1976

Bovine leukemia virus: an exogenous RNA oncogenic virus.

Short-term cultures of bovine leukemic lymphocytes release virus particles with biochemical properties of RNA oncogenic viruses. These particles, tentatively called bovine leukemia virus (BLV), have a high molecular weight RNA-reverse transcriptase complex and a density of 1.155 g/ml in sucrose solutions. Molecular hybridizations between BLV/[3H]cDNA and several viral RNAs show that BLV is not related to Mason-Pfizer monkey virus, simian sarcoma associated virus, feline leukemia virus, or avian myeloblastosis virus. These results were confirmed by hybridization between BLV 70S RNA and [3H]cDNA synthesized in the various viruses tested. The high preference of BLV reverse transciptase for Mg++ as the divalent cation suggests that BLV might be an atypical mammalian leukemogenic "type C" virus. DNA-DNA hybridization studies using BLV [3H]cDNA as a probe strongly suggest that the DNA of bovine leukemic cells contains viral sequences that cannot be detected in normal bovine DNA.

Animals↗
PubMedDate not supplied

[Formation of transfecting DNA in acute cellular infection with the tick-borne encephalitis virus mediated by an oncogenic virus].

To prove the association of the transfecting activity of nucleic acid from cells co-infected with TBE and SV40 viruses with DNA, experiments were carried out using fractionation of nucleic acid preparations in cesium sulphate gradient an on a column with HAP. The experiments led to a conclusion that the infectivity of the preparations used was associated with double-stranded DNA. Investigation of nucleic acid infectivity form cytochalasine-enucleated cells indicated that the function of the nucleus was necessary for formation of transfecting DNA in mixed TBE and SV40 infection of cell. No formation of transfecting DNA was observed in experiments of blocking replication and transcription of cellular genome. The retention of the transfecting activity of DNA during 6 passages of cells at approximately the same level indicated the lack of selective preferences or inhibition of cells containing transfecting DNA.

Acute Disease↗
PubMed1976

Evaluation of Moloney murine sarcoma and leukemia virus complex as a model for airborne oncogenic virus biohazards: survival of airborne virus and exposure of mice.

Aerosols of the Moloney murine sarcoma virus (MuSV-M) and leukemia virus (MuLV-M) complex (MuSV-M/MuLV-M) were generated from refluxing atomizers and then aged in rotating drums at 21 degrees C holding temperature with relative humidities ranging from 25 to 76%. The MuSV-M and MuLV-M aerosolized from the same tumor extract preparation survived almost equally at the four humidity levels. Both viruses remained viable in the airborne state for at least 2 hours after aerosolization. When mice were exposed to airborne MuSV-M/MuLV-M, no macroscopic lesions were observed in lungs or other tissues examined during the 2-month postexposure period. On the basis of this study, MuSV-M was determined unsuitable as a "model system" in which a simple aerosol dose response could be used for biohazard evaluation of oncogenic virus aerosols.

Aerosols↗
PubMed1999

Human DNA oncogenic viruses and their transforming protein interactions with cell cycle control proteins.

PURPOSE: Both oncogenic viruses and cell cycle control proteins are fast-growth research areas. More and more evidence indicates that virus infection and replication are often associated with apoptosis and interfere with cell cycle pathways. To understand the mechanisms by which viral proteins regulate apoptosis and target the cellular pathways may lead to the development of new remedies for some cancers. DATA SOURCES: English literature searched by MEDLINE from January 1995 to August 1998. STUDY SELECTION AND DATA EXTRACTION: More than one hundred research papers published in these areas over the past three years. Only new and important breakthroughs in these papers are selected. The review focuses on DNA viruses associated with the development of human cancers. RESULTS AND CONCLUSIONS: Some DNA viruses contain oncogenic proteins which transform normal cells in vitro and induce tumors in animals. These viral proteins target the cellular pathways and block apoptosis induced by receptors or in response to signal transduction. Viral interference with host cell apoptosis leads to enhanced viral replication and may promote carcinogenesis. Oncogenes and tumor suppressor genes, such as Retinoblastoma (RB) and p53, play important roles in regulation of these interactions.

Animals↗