Papovavirus-related RNA sequences in human neurogenic tumours

Ibelgaufts, Horst; Jones, Kenneth W.

doi:10.1007/bf00690582

Cited by 29 publications

(14 citation statements)

References 24 publications

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“…A papovavirus antigen has been identified in human meningiomas [73], and DNA hybridization techniques have found BK viral DNA, SV-40 viral DNA, and adenovirus DNA within meningiomas [75][76][77].…”

Section: Virusesmentioning

confidence: 99%

Epidemiology and etiology of intracranial meningiomas: A review

1996

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The frequency of meningiomas has been the topic of relatively few reports. Hospital-based brain tumor series indicate that the incidence is approximately 20% of all intracranial tumors; population-based studies indicate an overall incidence of 2.3/100,000. Although intracranial tumors as a whole show a higher prevalence in males than in females, meningiomas have a 2:1 female-to-male ratio. Between Caucasians and Africans, African-Americans, and Asians, certain differences also have been noted. Meningiomas in children are rare and differ from those in adults and other childhood tumors; they are even more rare in infants. Several features indicating etiologic factors have been identified, among which are ionizing radiation, head injury, hormones, and other receptor binding sites, genetic factors, and viruses. The most common source of exposure of the head to ionizing radiation is dental radiographic examination. Since 1922, head trauma has been considered a possible risk factor, but recent large studies do not support this link. Several factors have prompted studies of estrogens and progestogens as risk factors for meningiomas. Other studies have sought to determine if certain individuals have an inherited predisposition for developing a meningioma and/or if viruses, which may act alone or with other mutagens, figure into the formation of a meningioma. The most promising studies are those of cytogenetics, and future elucidation of factors associated with the loss of one copy of chromosome 22, another phenomenon that has been identified in meningiomas, may lead to screening tests and gene therapy.

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Section: Virusesmentioning

confidence: 99%

Epidemiology and etiology of intracranial meningiomas: A review

1996

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“…Although the demonstration of polyomavirusrelated nucleic acid sequences has been reported in a number of human neural tumors (124)(125)(126), the actual development of gliomas in the centers of the demyelinating lesions of PML has so far been limited to two well-documented reports (127,128), but it is of significance that in both instances the astrocytomas were multiple. That the JC strain of human polyomavirus is potentially capable of transforming human astrocytes would seem likely, but the hypothesis that some gliomas might be due to a nonpermissive infection of astrocytes by the virus of PML remains unproven.…”

Section: Progressive Multifocal Leukoencephalopathymentioning

confidence: 99%

The correlation of neoplastic vulnerability with central neuroepithelial cytogeny and glioma differentiation

Rubinstein

1987

J Neuro-Oncol

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The vulnerability of neuroepithelial cells in the central nervous system (CNS) to neoplastic transformation results from the interaction of several factors: the existence of a reserve population of stem cells, the capability of differentiated cells to reenter the kinetic cycle, the number of replicating cells at risk at a particular time, the length of time during which a particular cell population remains in the cycle, the state of differentiation and the further differentiation potential of that population, and the steps of differentiation that are achieved in successive cell generations. This concept explains many aspects of CNS tumor incidence and the relationship of central neuroepithelial embryonal tumors to tumors of adult cell type. The incidence of different types of central neuroepithelial tumors can be correlated with the width of the window of neoplastic vulnerability. Examples illustrating the existence of only a narrow window include such rare tumors as medulloepitheliomas, cerebral neuroblastomas, gangliogliomas and ependymoblastomas. By contrast, cerebellar medulloblastomas, astrocytomas, mixed astrocytomas and oligodendrogliomas, and glioblastomas exemplify instances in which a relatively wider window of vulnerability exists in the light of cellular neuro-ontogeny and of the capacity of glial cells for postnatal replication. The relationship that may occasionally be established between the development of a glioma and the production of cellular gliosis such as may follow brain injury or accompany multiple sclerosis can also be viewed in the light of that concept. Increasing awareness is needed concerning the development of postradiation gliomas, in particular after the apparently successful treatment of acute lymphocytic leukemia.

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“…The history of SV40 and its role in the development of primary brain cancers began soon after its discovery in 1960 when it was demonstrated to induce central nervous system malignancies following injection into newborn hamsters (Eddy et al, 1962;Girardi et al, 1962). Human studies conducted in the 1970s and 1980s identified SV40-positive brain tumors using DNA hybridization techniques or indirect immunofluorescence for viral proteins (Weiss et al, 1975;Tabuchi et al, 1978;Meinke et al, 1979;Krieg et al, 1981;Ibelgaufts and Jones, 1982;Dorries et al, 1987), whereas studies performed in the 1990s and 2000s generally used PCR-based approaches (Bergsagel et al, 1992;Martini et al, 1996;Suzuki et al, 1997;Huang et al, 1999;Krynska et al, 1999;Zhen et al, 1999;Ohgaki et al, 2000;Weggen et al, 2000;Kouhata et al, 2001;Malkin et al, 2001;Engels et al, 2002;Martini et al, 2002).…”

Section: Primary Brain Cancersmentioning

confidence: 99%

“…In all, 11 studies fulfilled the criteria among 16 articles reporting on SV40 and primary human brain cancers through November 2001 (Figure 1) (Weiss et al, 1975;Meinke et al, 1979;Krieg et al, 1981;Ibelgaufts and Jones, 1982;Dorries et al, 1987;Bergsagel et al, 1992;Martini et al, 1996;Suzuki et al, 1997;Zhen et al, 1999;Weggen et al, 2000;Malkin et al, 2001). The adjusted combined effect size (odds ratio (OR)) of the 11 original studies was 3.9 (95% confidence interval (CI), 6-8).…”

Section: Primary Brain Cancersmentioning

confidence: 99%

“…The effect (OR) was based on a total of 1003 samples, of which 589 were primary brain cancer samples and 414 were control samples. Five studies assessed the presence of SV40 in brain cancers by initial PCR (Bergsagel et al, 1992;Martini et al, 1996;Suzuki et al, 1997;Weggen et al, 2000;Malkin et al, 2001), four by DNA hybridization techniques (Meinke et al, 1979;Krieg et al, 1981;Ibelgaufts and Jones, 1982;Dorries et al, 1987), one by indirect immunofluorescence (Weiss et al, 1975), and one by immunoprecipitation (Zhen et al, 1999). Seven studies included only noncancer control samples (Meinke et al, 1979;Krieg et al, 1981;Dorries et al, 1987;Martini et al, 1996;Suzuki et al, 1997;Zhen et al, 1999;Malkin et al, 2001), and four studies included both noncancer and cancer control samples (Weiss et al, 1975;Ibelgaufts and Jones, 1982;Bergsagel et al, 1992;Weggen et al, 2000).…”

Section: Primary Brain Cancersmentioning

confidence: 99%

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SV40 in human brain cancers and non-Hodgkin's lymphoma

Vilchez

Butel

2003

Oncogene

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Simian virus 40 (SV40) is a potent DNA tumor virus that is known to induce primary brain cancers and lymphomas in laboratory animals. SV40 oncogenesis is mediated by the viral large tumor antigen (T-ag), which inactivates the tumor-suppressor proteins p53 and pRb family members. During the last decade, independent studies using different molecular biology techniques have shown the presence of SV40 DNA, T-ag, or other viral markers in primary human brain cancers, and a systematic assessment of the data indicates that the virus is significantly associated with this group of human tumors. In addition, recent large independent studies showed that SV40 T-ag DNA is significantly associated with human non-Hodgkin's lymphoma (NHL). Although the prevalence of SV40 infections in humans is not known, numerous observations suggest that SV40 is a pathogen in the human population today. This review examines the molecular biology, pathology, and clinical data implicating SV40 in the pathogenesis of primary human brain cancers and NHL and discusses future research directions needed to define a possible etiologic role for SV40 in these malignancies.

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Papovavirus-related RNA sequences in human neurogenic tumours

Cited by 29 publications

References 24 publications

Epidemiology and etiology of intracranial meningiomas: A review

Epidemiology and etiology of intracranial meningiomas: A review

The correlation of neoplastic vulnerability with central neuroepithelial cytogeny and glioma differentiation

SV40 in human brain cancers and non-Hodgkin's lymphoma

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