1992
DOI: 10.1016/0964-1955(92)90044-2
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In vitro and animal studies of the role of viruses in oral carcinogenesis

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Cited by 34 publications
(9 citation statements)
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“…Integration of HPV DNA into the human cellular genome is an important step for malignant transformation. Molecular studies have shown that high-risk HPV integration results in production of the viral oncoproteins E6 and E7, which promote tumour progression by inactivating the p53 gene and retinoblastoma tumour-suppressor gene products, respectively [122,123,124,125]. Using a qualitative PCR method, detection of HPV DNA in saliva rinses was examined and its association with HPV in tissue specimens was reported.…”
Section: Oral Cancermentioning
confidence: 99%
“…Integration of HPV DNA into the human cellular genome is an important step for malignant transformation. Molecular studies have shown that high-risk HPV integration results in production of the viral oncoproteins E6 and E7, which promote tumour progression by inactivating the p53 gene and retinoblastoma tumour-suppressor gene products, respectively [122,123,124,125]. Using a qualitative PCR method, detection of HPV DNA in saliva rinses was examined and its association with HPV in tissue specimens was reported.…”
Section: Oral Cancermentioning
confidence: 99%
“…17 Primary HSV infection is followed by latent viral infection in the ganglia. 17 According to the ''skin trigger theory,'' individuals with latent HSV infection in the ganglia actively shed infectious virions to peripheral sites with or without clinical symptoms 17 ; Kaufman et al 18 reported that the percentage of asymptomatic subjects who intermittently shed HSV-1 DNA in tears or saliva was higher than the percentage of subjects with positive neutralization antibodies to HSV. The repeated exposure of the cells to the virus could induce certain molecular changes in those cells and provide an opportunity for HSV to interact with environmental factors such as UV light.…”
Section: Discussionmentioning
confidence: 99%
“…Pour certains auteurs, ils agiraient en entraînant soit une mutation de TP53, soit une inactivation des protéines p53 et Rb par l'intermédiaire de 2 oncoprotéines virales E6 et E7 [53]. Pour d'autres auteurs, ils n'interviendraient que comme cocarcinogènes [54]. Même si les études ne sont pas unanimes quant à la participation de l'HPV dans la cancérogenèse des carcinomes des VADS, il est vraisemblable que cet agent infectieux rende compte d'une partie des carcinomes des VADS diagnostiqués chez les patients n'ayant pas d'intoxication alcoolotabagique (5 à 10 % en fonction des études) [40].…”
Section: Autres Facteurs De Risqueunclassified