2012
DOI: 10.1371/journal.ppat.1002807
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Abstract: The role of the E6 oncoprotein from high-risk members of the α human papillomavirus genus in anogenital cancer has been well established. However, far less is known about the E6 protein from the β human papillomavirus genus (β-HPVs). Some β-HPVs potentially play a role in non-melanoma skin cancer development, although they are not required for tumor maintenance. Instead, they may act as a co-factor that enhances the carcinogenic potential of UV damage. Indeed, the E6 protein from certain β-HPVs (HPV 5 and 8) p… Show more

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Cited by 126 publications
(181 citation statements)
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References 62 publications
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“…Instead, they may act as a cofactor that enhances the carcinogenic potential of UV damage, as shown by Wallace et al, 58 who also demonstrated that b-HPV E6 expression can enhance the carcinogenic potential of UV exposure by promoting p300 degradation.…”
Section: Modern Pathology (2014) 27 1101-1115mentioning
confidence: 99%
“…Instead, they may act as a cofactor that enhances the carcinogenic potential of UV damage, as shown by Wallace et al, 58 who also demonstrated that b-HPV E6 expression can enhance the carcinogenic potential of UV exposure by promoting p300 degradation.…”
Section: Modern Pathology (2014) 27 1101-1115mentioning
confidence: 99%
“…[42] Mainly, these tumors are induced by sun explosion and ultraviolet radiation. Cells with HPV5 and HPV8 E6 proteins disturb DNA double strand break repair [188] and reduces the efficiency of base excision repair pathway [189] causing higher sensitivity to UV-B exposure. It may be possible that because of impaired DNA repair activity, patients with acquired immunodeficiency syndrome or patients with epidermodysplasia verruciformis are more subjected for the infections and at a higher risk of developing HPV associated cutaneous malignancies.…”
Section: Skin Cancermentioning
confidence: 99%
“…30 Additionally, b-PV E6 targets the pro-apoptotic protein Bak for degradation. 31,32 These effects, usually combined with mechanisms that delay DNA repair (like abrogation of ATR activity 33 ) or impairment of the telomere/ telomerase system 34 may explain b-PV contribution to skin carcinogenesis by favoring the accumulation of UV damaged cells. The oncogenic potential of b-PV has also been shown in in vivo transgenic models which develop SCC in response to b-PV gene expression, either spontaneously or after UV irradiation.…”
Section: Introductionmentioning
confidence: 99%