2001
DOI: 10.1038/sj.onc.1204958
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Oncogenic DNA viruses

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Cited by 111 publications
(80 citation statements)
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References 36 publications
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“…HPV types 16,18,31,33,35,39,45,51,52,56,58,59,68,73 and 82 are considered as high risk types while 6,11,40,42,43,44,54,61,70,72,81 and CP6 108 as low risk types (Munoz et al, 2003). Among high risk HPV types, HPV 16 and 18 are considered to be carcinogenic agents and are strongly implicated with the development of cervical cancer (IARC Monographs Working Group, 1995;zur Hausen, 2001).…”
mentioning
confidence: 99%
“…HPV types 16,18,31,33,35,39,45,51,52,56,58,59,68,73 and 82 are considered as high risk types while 6,11,40,42,43,44,54,61,70,72,81 and CP6 108 as low risk types (Munoz et al, 2003). Among high risk HPV types, HPV 16 and 18 are considered to be carcinogenic agents and are strongly implicated with the development of cervical cancer (IARC Monographs Working Group, 1995;zur Hausen, 2001).…”
mentioning
confidence: 99%
“…To solve this problem, we should acknowledge that the classical Koch's postulates are not applicable to ubiquitous viruses that produce a persistent/latent infection. New rules should be considered for these viruses in order to establish their oncogenic role in humans (zur Hausen, 1994Hausen, , 2001Barbanti-Brodano et al, 1998): (i) presence and persistence of the virus or its nucleic acid in tumor cells; (ii) cell immortalization or neoplastic transformation after transfection of the viral genome or its subgenomic fragments; (iii) demonstration that the malignant phenotype of the primary tumor and the modifications induced by transfection of cultured cells depend on specific functions expressed by the viral genome; (iv) epidemiological and clinical evidence that viral infection represents a risk factor for tumor development. This review will show that BKV may fulfill at least the first three criteria and suggest that it may cooperate as a cofactor to the induction or progression of human tumors.…”
Section: Introductionmentioning
confidence: 99%
“…Based on the current understanding, it has been estimated that some 15% of the global cancer burden can be linked to oncogenic tumor viruses [20]. Various in vitro studies have demonstrated that the gene products of CMV are capable of modulating cell cycle progression and apoptosis by regulating the expression of a member of important host genes.…”
Section: Discussionmentioning
confidence: 99%