Immunodetection of SV40 large T antigen in human central nervous system tumours: Figure 1

Sabatier, Jean; Uro‐Coste, Emmanuelle; A, Benouaich; Boetto, S; Gigaud, M; Trémoulet, M; Mb, Delisle; Galateau-Sallé, Françoise; Brousset, Pierre

doi:10.1136/jcp.2004.020131

Cited by 12 publications

(7 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunodetection of T-Ag in human brain tumor panels has also yielded some negative reports. Sabatier et al recently reported that none of a French series of 82 CNS tumors was positive for T-Ag by immunohistochemistry (80). Of note, this study employed the same monoclonal antibody (Ab-2, clone Pab416, Oncogene Research, San Diego, CA) that was routinely used in immunohistochemistry of brain tumors with positive results (67, 68, 75, 76).…”

Section: Introductionmentioning

confidence: 99%

Potential Mechanisms of the Human Polyomavirus JC in Neural Oncogenesis

Valle

White

Khalili

2008

J Neuropathol Exp Neurol

View full text Add to dashboard Cite

The human polyomavirus JC (JCV) is a small DNA tumor virus and the etiological agent of the progressive multifocal leukoencephalopathy (PML). In PML, active JCV replication causes the lytic destruction of oligodendrocytes. The normal immune system prevents JCV replication and suppresses the virus into a state of latency so that expression of viral proteins cannot be detected. In a cellular context that is non-permissive for viral replication, JCV can effect oncogenic transformation. For example, JCV is highly tumorigenic when inoculated into experimental animals including rodents and monkeys. In these animal tumors there is expression of early T-antigen but not of late capsid proteins, nor is there viral replication. Moreover, mice transgenic for JCV T-antigen alone develop tumors of neural tube origin. Detection of JCV genomic sequences and expression of viral T-antigen and agnoprotein suggest a possible association of this virus with a variety of human brain and non-CNS tumors. Here, we discuss the mechanisms involved in JCV oncogenesis, briefly review studies that do and do not support a causative role for this virus in human CNS tumors and identify key issues for future research.

show abstract

Section: Introductionmentioning

confidence: 99%

Potential Mechanisms of the Human Polyomavirus JC in Neural Oncogenesis

Valle

White

Khalili

2008

J Neuropathol Exp Neurol

View full text Add to dashboard Cite

show abstract

“…This polyomavirus is known to induce brain tumors in hamsters; however, results of epidemiological studies of the effect of this virus on human brain tumor development remain conflictive. [6,7,30] Another virus investigated in a small number of brain tumor studies is the JC virus, which is a commonly active infection in immunosuppressed or immunodeficient patients and pregnant women. Khalili et al [21]recently detected JC virus in paraffin-embedded tumor tissue specimens obtained from children with medulloblastoma.…”

Section: Introductionmentioning

confidence: 99%

Detection of human cytomegalovirus in different histological types of gliomas

et al. 2008

View full text Add to dashboard Cite

The association between human cytomegalovirus (HCMV) infection and glioblastoma has been a source of debate in recent years because of conflicting laboratory reports concerning the presence of the virus in glioma tissue. HCMV is a ubiquitous herpesvirus that exhibits tropism for glial cells and has been shown to transform cells in vitro. Using sensitive immunohistochemical and in situ hybridization methods in 50 glioma samples, we detected HCMV antigen and DNA in 21/21 cases of glioblastoma, 9/12 cases of anaplastic gliomas, and 14/17 cases of low-grade gliomas. Reactivity against the HCMV IE1 antigen (72 kDa) exhibited histology-specific patterns with more nuclear staining for anaplastic and low-grade gliomas, while GBMs showed nuclear and cytoplasmic staining that likely occurs with latent infection. Using IHC, the number of HCMVpositive cells in GBMs was 79% compared to 48% in lower grade tumors. Non-tumor areas of the tissue contained only 4 % and 1% of HCMV-positive cells for GBMs and lower grade tumors, respectively. Hybridization to HCMV DNA in infected cells corresponded to patterns of immunoreactivity. Our findings support previous reports of the presence of HCMV infection in glioma tissues and advocate optimization of laboratory methods for the detection of active HCMV infections. This will allow for detection of low-level latent infections that may play an important role in the initiation and/or promotion of malignant gliomas.

show abstract

“…In any sample with viral cytopathic changes only (Pattern A), or in combination with tubular atrophy and interstitial inflammation and fibrosis (Pattern B), or where there was clinical suspicion of PVAN (e.g. because of prior positive PVPCR or otherwise unexplained deterioration in renal function), additional immunohistochemical staining for the presence of the polyomavirus SV40 antigen with a murine anti‐SV40 T antigen monoclonal antibody (Calbiochem® Anti‐SV40 T Antigen, PAb416; Merck, San Diego, CA, USA) was undertaken 27 . All specimens were examined by at least one pathologist experienced in renal transplant histology and scored according to the Banff classification 28 .…”

Section: Methodsmentioning

confidence: 99%