The presence of bovine papillomavirus type 4 DNA is not required for the progression to, or the maintenance of, the malignant state in cancers of the alimentary canal in cattle.

Campo, M. Saveria; Moar, Martin H.; Sartirana, M. L.; Kennedy, Iain M.; Jarrett, W. F. H.

doi:10.1002/j.1460-2075.1985.tb03856.x

Cited by 76 publications

(39 citation statements)

References 36 publications

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“…In addition, a low copy number of HPV DNA is usually associated with skin cancer, thus suggesting that it could be contained only in a minority of tumour [7]. The data so far obtained are more compatible with cutaneous HPVs being possibly involved in tumour initiation and progression, with a so-called "hit and run" mechanism of carcinogenesis, as already demonstrated for the BPV-4-associated oesophageal carcinoma [27]. In this respect, our biomolecular and immunohistochemical findings, indicative of low levels of PV DNA sequences and viral antigens expression, are in agreement with such hypothesis.…”

supporting

confidence: 69%

Papillomaviruses in Multiple Tumours of Twin Goats

Simeone¹,

Romanucci²,

Rizzo³

et al. 2008

TOVSJ

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supporting

confidence: 69%

Papillomaviruses in Multiple Tumours of Twin Goats

Simeone¹,

Romanucci²,

Rizzo³

et al. 2008

TOVSJ

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“…When tumor cells are removed from these animals and grown in culture, TAg expression is lost (25). A similar loss of oncoprotein expression is seen in cancers of the alimentary canal in cattle caused by bovine papillomavirus type 4: the virus is required for the induction of papillomas, but its presence is not necessary for progression or maintenance of the transformed state (11). Additional work will be required to determine if a causal connection between BKV and prostate cancer exists.…”

Section: Discussionmentioning

confidence: 88%

BK Virus as a Cofactor in the Etiology of Prostate Cancer in Its Early Stages

Das

Wojno²,

Imperiale

2008

J Virol

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Prostate cancer has been projected to cause almost 10% of all male cancer deaths in the United States in 2007. The incidence of mutations in the tumor suppressor genes Rb1 and p53, especially in the early stages of the disease, is low compared to those for other cancers. This has led to the hypothesis that a human virus such as BK virus (BKV), which establishes a persistent subclinical infection in the urinary tract and encodes oncoproteins that interfere with these tumor suppressor pathways, is involved. Previously, we detected BKV DNA in the epithelial cells of benign and proliferative inflammatory atrophy ducts of cancerous prostate specimens. In the present report, we demonstrate that BKV is present at a much lower frequency in noncancerous prostates. Additionally, in normal prostates, T-antigen (TAg) expression is observed only in specimens harboring proliferative inflammatory atrophy and prostatic intraepithelial neoplasia. We further demonstrate that the p53 gene from atrophic cells expressing TAg is wild type, whereas tumor cells expressing detectable nuclear p53 contain a mix of wild-type and mutant p53 genes, suggesting that TAg may inactivate p53 in the atrophic cells. Our results point toward a role for BKV in early prostate cancer progression.

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“…However, in keeping with the previous report using in situ hybridization (Snow et al, 1992), we could not detect HPV genome in any tumours examined. Therefore, the involvement of HPV in the tumorigenesis of extramammary Paget's disease seems unlikely, although there remains a possibility that a virus may play a 'hit and run' role in tumour pathogenesis (Campo et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Tumour cells of extramammary Paget's disease do not show either p53 mutation or allelic loss at several selected loci implicated in other cancers

Takata

Hatta²,

Takehara³

1997

Br J Cancer

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Summary Extramammary Paget's disease is a particular form of skin cancer of unknown histogenesis. To look for the genetic defects underlying the pathogenesis of this tumour, we have examined loss of heterozygosity (LOH), p53 and human papillomavirus (HPV) status, and the expression of c-erbB-2 and bcl-2 proteins in 14 cases. Unexpectedly, no LOH was detected at several loci commonly lost in other human cancers (namely 3p, 9p, 9q, 13q, 16q, 17p, and 17q) in 12 tumours examined. Altered p53 protein expression was entirely or mostly negative in all 14 cases. Direct sequencing of exons 5-8 of the p53 gene in eight cases revealed no mutation. Polymerase chain reaction amplification of the Ll gene of human papillomavirus (HPV) did not detect the virus that could inactivate p53 and retinoblastoma tumoursuppressor gene products. As expected, c-erbB-2 proto-oncogene protein was overexpressed in six cases. The expression of bcl-2 was negative in all cases. The results presented in this study suggest that molecular events underlying extramammary Paget's disease differ from those of other common epithelial malignancies and that tumour-suppressor genes located in chromosome regions not examined in this study may be important.

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The presence of bovine papillomavirus type 4 DNA is not required for the progression to, or the maintenance of, the malignant state in cancers of the alimentary canal in cattle.

Cited by 76 publications

References 36 publications

Papillomaviruses in Multiple Tumours of Twin Goats

Papillomaviruses in Multiple Tumours of Twin Goats

BK Virus as a Cofactor in the Etiology of Prostate Cancer in Its Early Stages

Tumour cells of extramammary Paget's disease do not show either p53 mutation or allelic loss at several selected loci implicated in other cancers

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