scholarly journals Simian virus 40 and cancer

2011 ◽  
pp. 131-140
Author(s):  
Sandra Eliasz ◽  
Michele Carbone ◽  
Maurizio Bocchetta
Keyword(s):  
Molecular Biology ◽  
Human Population ◽  
Animal Studies ◽  
Cell Transformation ◽  
Human Cancer ◽  
Mesothelial Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Oncogenic Virus ◽  
Experimental Approaches

Since its discovery in 1960 as a contaminant of poliovaccines, Simian Virus 40 (SV40) has been the object of extensive studies to assess whether this oncogenic virus plays a role in human carcinogenesis. Over the last two decades, this question has met with broad scepticism. However, there is increasing evidence linking SV40 to specific types of human cancer, especially malignant mesothelioma. Recently, two laboratories using different experimental approaches independently confirmed that SV40 acts synergistically with environmental fibers to promote mesothelial cell transformation and mesothelioma. Most of the scepticism concerning SV40 and cancer was due to the lack of clear epidemiologic data. However, it is still not clear how SV40 circulates in the human population, making the identification of SV40-exposed versus non-exposed cohorts problematic. Consequently, the most helpful insights into SV40-mediated carcinogenesis have come from molecular pathology, cell and molecular biology, and from animal studies.

scholarly journals More About: Cell and Molecular Biology of Simian Virus 40: Implications for Human Infections and Disease

2000 ◽  
Vol 92 (6) ◽  
pp. 495-496 ◽  
Author(s):  
Hiroko Ohgaki ◽  
Huatao Huang ◽  
Matti Haltia ◽  
Harri Vainio ◽  
Paul Kleihues
Keyword(s):  
Molecular Biology ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Human Infections

scholarly journals Investigation of the SV40 – Human Cancer Association: Look for the Full Signature of the Virus

2001 ◽  
Vol 17 (3) ◽  
pp. 159-161 ◽  
Author(s):  
Keerti V. Shah ◽  
Dana E. M. Rollison
Keyword(s):  
Risk Factors ◽  
Tumor Cell ◽  
Cancer Patients ◽  
Sensitivity And Specificity ◽  
Human Cancer ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Viral Integration ◽  
Human Community ◽  
Sv40 Infection

In the controversy about the association of simian virus 40 with human cancers, the greatest problem is the ascertainment of SV40 exposure. This difficulty would be resolved if one were to look for all components of SV40 infection. How does SV 40 circulate in the human community? Do cancer patients with SV40-positive tumors have serological correlates of SV 40 infection and of SV40-induced cancer? SV40 association with a cancer should be studied in the context of the known risk factors for that cancer. The tumor cell-virus relationship should be characterized with respect to viral integration and viral localization to the tumor cell. Specimens should be masked and the assays should include panels of specimens to estimate analytic sensitivity and specificity. In view of the rarity of some of the tumors reported to be associated with SV40, a multi-institutional investigation initiated and coordinated by the NIH would be most effective.

scholarly journals Enumeration of the Simian Virus 40 Early Region Elements Necessary for Human Cell Transformation

2002 ◽  
Vol 22 (7) ◽  
pp. 2111-2123 ◽  
Author(s):  
William C. Hahn ◽  
Scott K. Dessain ◽  
Mary W. Brooks ◽  
Jessie E. King ◽  
Brian Elenbaas ◽  
...  
Keyword(s):  
Cell Transformation ◽  
Human Tumor ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Experimental Models ◽  
T Antigen ◽  
Human Cells ◽  
Sv40 Large T Antigen ◽  
Early Region ◽  
Intracellular Pathways

ABSTRACT While it is clear that cancer arises from the accumulation of genetic mutations that endow the malignant cell with the properties of uncontrolled growth and proliferation, the precise combinations of mutations that program human tumor cell growth remain unknown. The study of the transforming proteins derived from DNA tumor viruses in experimental models of transformation has provided fundamental insights into the process of cell transformation. We recently reported that coexpression of the simian virus 40 (SV40) early region (ER), the gene encoding the telomerase catalytic subunit (hTERT), and an oncogenic allele of the H-ras gene in normal human fibroblast, kidney epithelial, and mammary epithelial cells converted these cells to a tumorigenic state. Here we show that the SV40 ER contributes to tumorigenic transformation in the presence of hTERT and oncogenic H-ras by perturbing three intracellular pathways through the actions of the SV40 large T antigen (LT) and the SV40 small t antigen (ST). LT simultaneously disables the retinoblastoma (pRB) and p53 tumor suppressor pathways; however, complete transformation of human cells requires the additional perturbation of protein phosphatase 2A by ST. Expression of ST in this setting stimulates cell proliferation, permits anchorage-independent growth, and confers increased resistance to nutrient deprivation. Taken together, these observations define the elements of the SV40 ER required for the transformation of human cells and begin to delineate a set of intracellular pathways whose disruption, in aggregate, appears to be necessary to generate tumorigenic human cells.

scholarly journals Elevated recombination in immortal human cells is mediated by HsRAD51 recombinase.

1997 ◽  
Vol 17 (12) ◽  
pp. 7151-7158 ◽  
Author(s):  
S J Xia ◽  
M A Shammas ◽  
R J Shmookler Reis
Keyword(s):  
Cell Lines ◽  
Cell Transformation ◽  
Human Fibroblasts ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Cell Strains ◽  
Immortal Cells ◽  
Diploid Cells ◽  
Untransformed Cell

Normal diploid cells have a limited replicative potential in culture, with progressively increasing interdivision time. Rarely, cell lines arise which can divide indefinitely; like tumor cells, such "immortal" lines display frequent chromosomal aberrations which may reflect high rates of recombination. Recombination frequencies within a plasmid substrate were 3.5-fold higher in nine immortal human cell lines than in six untransformed cell strains. Expression of HsRAD51, a human homolog of the yeast RAD51 and Escherichia coli recA recombinase genes, was 4.5-fold higher in immortal cell lines than in mortal cells. Stable transformation of human fibroblasts with simian virus 40 large T antigen prior to cell immortalization increased both chromosomal recombination and the level of HsRAD51 transcripts by two- to fivefold. T-antigen induction of recombination was efficiently blocked by introduction of HsRAD51 antisense (but not control) oligonucleotides spanning the initiation codon, implying that HsRAD51 expression mediates augmented recombination. Since p53 binds and inactivates HsRAD51, T-antigen-p53 association may block such inactivation and liberate HsRAD51. Upregulation of HsRAD51 transcripts in T-antigen-transformed and other immortal cells suggests that recombinase activation can also occur at the RNA level and may facilitate cell transformation to immortality.

Simian virus 40(SV40) and human cancer: a review of the serological data

2004 ◽  
Vol 14 (4) ◽  
pp. 231-239 ◽  
Author(s):  
Keerti V. Shah ◽  
Denise A. Galloway ◽  
Wendy A. Knowles ◽  
Raphael P. Viscidi
Keyword(s):  
Human Cancer ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Serological Data
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