Hypothesis: "Rogue cell"-type chromosomal damage in lymphocytes is associated with infection with the JC human polyoma virus and has implications for oncopenesis.

Neel, James V.; Major, Eugene O.; Awa, Akio A.; Glover, TW; Burgess, Ann C.; Traub, Renee G.; Curfman, Blanche; Satoh, Chiyoko

doi:10.1073/pnas.93.7.2690

Cited by 99 publications

(66 citation statements)

References 31 publications

(29 reference statements)

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“…This search led to the discovery of the archetype regulatory region. Derived from virus in kidney tissue [82,96,97] and urine [60,[62][63][64][65][66][67][68]74], archetype singularly contained all the nucleotide elements found in repeat structures. The limited biological activity of the archetype regulatory region, however, led to debate concerning the roles of JCV variants in PML pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Other studies have linked JCV with cancers of the human immune system. Individuals exhibiting ''rogue cell'' chromosomal aberrations among their cultured lymphocytes were shown to have high HI titers for JCV specific antibodies [66,67]. In addition, some lines of evidence point to JCV as the etiologic agent responsible for active lymphoblastic leukemia (ALL) in children [68].…”

Section: Implications Of Oncogenicitymentioning

confidence: 99%

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Viral variant nucleotide sequences help expose leukocytic positioning in the JC virus pathway to the CNS

Jensen

Major

1999

Journal of Leukocyte Biology

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Section: Discussionmentioning

confidence: 99%

Section: Implications Of Oncogenicitymentioning

confidence: 99%

Viral variant nucleotide sequences help expose leukocytic positioning in the JC virus pathway to the CNS

Jensen

Major

1999

Journal of Leukocyte Biology

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“…The immune serum anti-BKV was titered by the hemagglutination inhibition test using human erythrocytes from the 0, Rh + group (55,58). Anti-SV40 serum was titered by neutralization assay (54,59).…”

Section: Sv40 Mimotopesmentioning

confidence: 99%

High prevalence of serum antibodies reacting with simian virus 40 capsid protein mimotopes in patients affected by malignant pleural mesothelioma

Mazzoni¹,

Corallini

Cristaudo

et al. 2012

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

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Human malignant pleural mesothelioma (MPM) is considered a rare tumor, but recent estimations indicate that one-quarter million people will die of this neoplasm in Europe in the next three decades. The mineral asbestos is considered the main causative agent of this neoplasm. MPM is largely unresponsive to conventional chemotherapy/radiotherapy. In addition to asbestos exposure, genetic predisposition to asbestos carcinogenesis and to simian virus (SV) 40 infection has also been suggested. SV40 is a DNA tumor virus found in some studies to be associated at high prevalence with MPM. SV40 sequences have also been detected, although at a lower prevalence than in MPM, in blood specimens from healthy donors. However, some studies have failed to reveal SV40 footprints in MPM and its association with this neoplasm. These conflicting results indicate the need for further investigations with new approaches. We report on the presence of antibodies in serum samples from patients affected by MPM that specifically react with two different SV40 mimotopes. The two SV40 peptides used in indirect ELISAs correspond to viral capsid proteins. ELISA with the two SV40 mimotopes gave overlapping results. Our data indicate that in serum samples from MPM-affected patients (n = 97), the prevalence of antibodies against SV40 viral capsid protein antigens is significantly higher (26%, P = 0.043) than in the control group (15%) represented by healthy subjects (n = 168) with the same median age (66 y) and sex. Our results suggest that SV40 is associated with a subset of MPM and circulates in humans.antibody | neoplasia

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“…Immunohistochemical staining for JCV T-antigen shows positive staining in the nuclei of tumor cells in all three tumor types (panels c, f, and i, respectively). (panels a, d, and G: hematoxylin and eosin staining; panels b, c, e, f, h, and i: hematoxylin counterstain; All panels: original magnification Â 400) Lazutka et al, 1996;Neel et al, 1996). In further evidence of the ability of T-antigen to induce alterations at the chromosome level, morphological changes such as multinucleation, high nuclear pleomorphism, aneuploidy, and polyploidy have been observed in T-antigeninduced transgenic mouse tumors and cell cultures derived from those tumors (Krynska et al, 2000;Gordon et al, unpublished observations).…”

Section: Mechanisms Of T-antigen-mediated Transformationmentioning

confidence: 99%

Human neurotropic polyomavirus, JCV, and its role in carcinogenesis

et al. 2003

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A number of recent studies have reported the detection of the ubiquitous human polyomavirus, JC virus (JCV), in samples derived from several types of neural as well as non-neural human tumors. The human neurotropic JCV was first identified as the etiologic agent of the fatal demyelinating disease, progressive multifocal leukoencephalopathy, which usually occurs in individuals with defects in cell-mediated immunity, including AIDS. However, upon mounting evidence of the oncogenic potential of the viral regulatory protein, T-antigen, and JCV's oncogenecity in a broad range of animal models, studies were initiated to determine its potential involvement in human carcinogenesis. Initially, the most frequently observed tumors in rodent models, including medulloblastoma, astrocytoma, glioblastoma, and other neural-origin tumors were analysed. These studies were followed by analysis of non-neural tumors such as colorectal carcinomas. In a subset of each tumor type examined, JC viral genomic DNA sequences could be detected by PCR and confirmed by Southern blot hybridization or direct sequencing. In a smaller subset of the tumors, the expression of T-antigen was observed by immunohistochemical analysis. Owing to the established functions of T-antigen including its ability to interact with tumor suppressor proteins such as Rb and p53, and its ability to influence chromosomal stability, potential mechanisms of JCV T-antigen-mediated cellular dysregulation are discussed. Further, as increasing evidence suggests that T-antigen is not required for maintenance of a transformed phenotype, a hit-and-run model for T-antigen-induced transformation is proposed.

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Hypothesis: "Rogue cell"-type chromosomal damage in lymphocytes is associated with infection with the JC human polyoma virus and has implications for oncopenesis.

Abstract: The hemagglutination inhibition antibody titers against the JC and BK polyoma viruses (JCV and BKV, respectively)

Cited by 99 publications

References 31 publications

Viral variant nucleotide sequences help expose leukocytic positioning in the JC virus pathway to the CNS

Viral variant nucleotide sequences help expose leukocytic positioning in the JC virus pathway to the CNS

High prevalence of serum antibodies reacting with simian virus 40 capsid protein mimotopes in patients affected by malignant pleural mesothelioma

Human neurotropic polyomavirus, JCV, and its role in carcinogenesis

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