Induction of Lymphocytic Leukemia, Lymphosarcoma, Reticulum Cell Sarcoma, and Osteogenic Sarcoma in the Syrian Golden Hamster by Oncogenic DNA Simian Virus 40
            2

Diamandopoulos, George Th.

doi:10.1093/jnci/50.5.1347

Cited by 76 publications

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“…Furthermore, in animal models of SV40 induced neopla-sia, SV40 T-antigen is expressed in all malignant cells. 52 In vitro, repression of SV40 T-antigen function results in cellular senescence and loss of the transformed phenotype, 53 suggesting that a clonal-association with one or more copies of the SV40 Tantigen per tumor cell would be causally necessary. Previous studies that used quantitative PCR for detection of SV40 sequences in human tumors reported SV40 copy numbers substantially less than one viral copy per cell (1-100 copies per 0.5 lg of tumor DNA) 54 ; 0.12 in 14,000 cells, 55,56 or have been negative.…”

Section: Discussionmentioning

confidence: 99%

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

Gillison¹,

Chen²,

Goshu³

et al. 2007

Intl Journal of Cancer

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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 5 1), bilateral nonfamilial (n 5 1) and unilateral nonfamilial (n 5 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. ' 2006 Wiley-Liss, Inc.Key words: human papillomavirus; retinoblastoma; virus; causation Retinoblastoma is a rare childhood cancer of the retina, classically initiated by loss or mutation of both alleles of the retinoblastoma gene (RB1) during retinal development. Children with an inherited or de novo germline mutation in the RB1 gene develop bilateral or unilateral retinoblastoma with high penetrance, accounting for 40% of cases. In the majority of remaining cases, unilateral tumors occur as a consequence of somatic mutations that inactivate both RB1 alleles. Upon detailed analysis, mutations of the RB1 promoter or coding region can be identified in 92% of suspected RB1 alleles either as heterozygous germline mutations in heritable cases or as biallelic mutations in retinoblastoma tumors. 1 However, no RB1 inactivating event has been identified in 8% of RB1 alleles, leaving open the possibility that some retinoblastomas may be caused by alternative genetic or epigenetic events that modify retinoblastoma protein (pRB) function.The RB1 gene on chromosome 13q14 encodes a nuclear phosphoprotein (the tumor suppressor pRb) that plays a key regulatory role in the cell cycle check point between G1 and entry into Sphase. 2 In addition to mutations in the RB1 gene, pRb function can be abrogated by oncoproteins from several DNA tum...

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Section: Discussionmentioning

confidence: 99%

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

Gillison¹,

Chen²,

Goshu³

et al. 2007

Intl Journal of Cancer

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“…The nature of interaction of SV40 with lymphoid tissue is unclear. Bcell lymphomas occur in small-animal models of SV40 infection (Cicala et al, 1992;Diamandopoulos, 1973;Matthews et al, 1987), and SV40 is associated with some B-cell lymphomas in humans (Amara et al, 2007;David et al, 2001;Meneses et al, 2005;Shivapurkar et al, 2002;Vilchez et al, 2002b;Zekri et al, 2007). Therefore, B-cell-rich tissues such as tonsils may represent a site that harbors SV40.…”

Section: Introductionmentioning

confidence: 99%

Detection of polyomavirus SV40 in tonsils from immunocompetent children

Patel

Vilchez

Killen

et al. 2008

Journal of Clinical Virology

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Background-BK virus (BKV), JC virus (JCV) and simian virus 40 (SV40) are nonenveloped DNA viruses, members of the family Polyomaviridae. BK and JC viruses establish persistent infections in humans, and evidence suggests that SV40 can infect humans, as well. Whether persistence occurs in the lymphoid system is unknown.Methods-Paraffin-embedded tonsils from 220 immunocompetent children (mean age 9.3 years) were examined by polymerase chain reaction (PCR) to detect viral DNA of BKV, JCV, SV40, and Epstein-Barr virus (EBV).Results-Polyomavirus-specific DNA sequences were detected in 8.3% (29/351) of specimens collected from 220 children. Twenty-one (9.5%) children had polyomavirus DNA present in at least one tonsil, with sequences identified as SV40 (n=20) and BKV (n=1). Polyomavirus JCV was not detected. Among patients positive for SV40, 8 of 14 (57%) contained viral DNA in both available tonsils. EBV DNA was detected in 99 (28.2%) samples from 67 (30.5%) patients. Eleven samples (3.1%) from 8 (3.6%) children were positive for both polyomavirus and EBV. SV40-positive children were significantly older than the SV40-negative subjects (P < 0.001). T-antigen expression was detected in an SV40 DNA-positive tonsil by immunohistochemistry.Conclusions-These results suggest that SV40 can infect tonsils, that lymphoid tissue may represent a site for polyomavirus persistence, and that immunohistochemistry is not a useful detection assay when there are very few virus-infected cells in a tissue.

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“…To study this, suspensions containing 10 X 106 neoplastic lymphocytes derived from a hamster's subcutaneous tumor transplant at its 18th in vivo passage (Fig. 1B), were intermixed with 5 X 106 nucleated cells derived from its own non-leukemia-involved spleen before they were inoculated subcutaneously in each of 10 antiserum to SV40 (13) and by identifying SV40 T antigen in the neoplastic lymphocytes and antibody production against SV40 T antigen in hamsters bearing the primary neoplasms or their tumor transplants (13,22,23). Since all the lymphocytic neoplasms thus produced were of B-cell origin and lacked serologic markers for oncogenic RNA viruses (13), it follows that the role of SV40 in their induction is primary and essential.…”

Section: Resultsmentioning

confidence: 99%

“…1B), were intermixed with 5 X 106 nucleated cells derived from its own non-leukemia-involved spleen before they were inoculated subcutaneously in each of 10 antiserum to SV40 (13) and by identifying SV40 T antigen in the neoplastic lymphocytes and antibody production against SV40 T antigen in hamsters bearing the primary neoplasms or their tumor transplants (13,22,23). Since all the lymphocytic neoplasms thus produced were of B-cell origin and lacked serologic markers for oncogenic RNA viruses (13), it follows that the role of SV40 in their induction is primary and essential. Murine Although the primary neoplasm manifested itself as generalized lymphocytic leukemia rather than as localized lymphocytic lymphoma, the neoplastic lymphocytes lost their capacity to induce leukemia soon after they were transplanted subcutaneously in allogeneic animals.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Differences in behavior and prognosis between leukemic and lymphomatous forms of a transplantable hamster lymphocytic neoplasm induced by simian virus 40.

Diamandopoulos¹

1978

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

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Induction of Lymphocytic Leukemia, Lymphosarcoma, Reticulum Cell Sarcoma, and Osteogenic Sarcoma in the Syrian Golden Hamster by Oncogenic DNA Simian Virus 40 2

Cited by 76 publications

References 0 publications

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

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

Detection of polyomavirus SV40 in tonsils from immunocompetent children

Differences in behavior and prognosis between leukemic and lymphomatous forms of a transplantable hamster lymphocytic neoplasm induced by simian virus 40.

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