Human papillomaviruses in non-melanoma skin cancer

Villiers, Ethel Michele De; Ruhland, Astrid; Šekaric, Pedja

doi:10.1006/scbi.1999.0145

Cited by 47 publications

(45 citation statements)

References 90 publications

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“…Studies have shown that 90% of tumours in EV patients show the presence of HPVs, particularly types 5 and 8, which are commonly referred to as EV-associated types (Orth, 1986). RTR patients are instead subject to mixed infection with many different cutaneous types, including the recently isolated type HPV 77 (Delius et al, 1998;Surentheran et al, 1998;de Villiers et al, 1999;Harwood et al, 2000). It is important to note that although the EV types are included in the cutaneous group, they are distant phylogenetically from other cutaneous types and it has recently been argued that they may define a distinct subgroup within the cutaneous branch (Orth et al, 2001).…”

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confidence: 99%

RETRACTED ARTICLE: Human papillomavirus type 77 E6 protein selectively inhibits p53-dependent transcription of proapoptotic genes following UV-B irradiation

et al. 2004

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DNA damage, such as that elicited by UV-B, can induce either a cell cycle arrest or apoptosis that can be signalled by the p53 protein through the activation of a number of downstream cellular target genes. In contrast to oncogenic anogenital human papillomaviruses (HPVs), which mediate proteolytic degradation of p53, the E6 protein of cutaneous HPVs, such as HPV 77, do not promote p53 degradation. We have previously shown, however, that expression of HPV 77 E6 can effectively block UV-induced apoptosis in cells that have UV-activated p53. Here, we report that expression of the E6 protein from the cutaneous HPV 77 attenuates the UV-induced transactivation of p53-regulated proapoptotic genes Fas, PUMAb, Apaf-1, PIG3. This inhibition of p53-activation of proapoptotic genes by HPV77 E6 is exerted selectively, as the increased expression of p53 target genes involved in cell cycle arrest or regulatory functions regulation, such as p21 and Hdm2, is unaffected. Our data suggest that HPV 77 E6 may play an important role in specifically deregulating p53-dependent transactivation of proapoptotic genes upon UV-B irradiation.

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confidence: 99%

RETRACTED ARTICLE: Human papillomavirus type 77 E6 protein selectively inhibits p53-dependent transcription of proapoptotic genes following UV-B irradiation

et al. 2004

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“…32 These cutaneaous HPVs are phylogentically and also probably pathologically and biologically different from the causal mucosal types in anogenital and upper aerodigestive tract cancers. 33 The lack of aggregation of skin SCCs with cancers at other sites in our study may reflect site-specific cofactors of HPV in carcinogenesis, such as cigarette smoking in anogenital and upper aerodigestive tract cancers and ultraviolet radiation in skin SCC, or differences in the biology or pathology of, or immune response to, the relevant HPV types.…”

Section: Discussionmentioning

confidence: 66%

Familial clustering of cancer at human papillomavirus‐associated sites according to the Swedish Family‐Cancer Database

Hussain

Sundquist

Hemminki

2007

Intl Journal of Cancer

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Familial aggregation of cervical cancer has been demonstrated previously, however aggregation of other human papillomavirus‐associated anogenital, upper aerodigestive tract and skin cancers has not been fully characterized. The Swedish Family‐Cancer Database, which contains reliable data on cancer incidence and nuclear family linkages for all residents of Sweden between 1958 and 2004, was used to calculate standardized incidence ratios (SIR) and 95% confidence intervals for offspring site‐specific cancer risks according to site‐specific cancer in sibling and parental probands. Offspring cancer risk was significantly increased when either a sibling or parent was affected at the same site for penile squamous cell carcinoma (SCC, SIR = 7.54), cervical adenocarcinoma (AC, SIR = 2.31), vulvar SCC (SIR = 2.27), skin SCC (SIR = 2.14), rectal AC (SIR = 1.86), in situ cervical SCC (SIR = 1.80), invasive cervical SCC (SIR = 1.77) and upper aerodigestive tract SCC (SIR = 1.57). Significant aggregation on the order of 2‐fold between anogenital cancers at different sites or histologies was also observed. In situ cervical SCC risk in offspring was strongly influenced by siblings affected with oropharyngeal SCC (SIR = 3.17) and tonsillar SCC (SIR = 1.84). Familial skin SCC was largely unassociated with anogenital or upper aerodigestive tract cancer risk in offspring. These data suggest that common host factors exist among individuals affected with anogenital and upper aerodigestive tract cancers. © 2007 Wiley‐Liss, Inc.

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“…The mechanistic role that individual viral proteins of the mucosal papillomaviruses play in the malignant conversion of genital keratinocytes has been described in detail (zur Hausen, 1996;Fehrmann and Laimins, 2003). In contrast, data on the mechanisms by which cutaneous papillomaviruses may function to influence cell proliferation and malignant progression (Jackson and Storey, 2000;Caldeira et al, 2003) or vice versa, the way by which external and cellular factors regulate the cutaneous papillomavirus activity (de Villiers et al, 1999;Ruhland and de Villiers, 2001) have been fractional.…”

Section: Discussionmentioning

confidence: 99%

“…Papillomavirus infections, ultraviolet irradiation and p53 mutations have been implicated in the pathogenesis of non-melanoma skin cancer (reviewed in de Villiers et al, 1999). Mutant p53 R248W has been shown to bind p63 via its core domain (Strano et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…The differential activity of the Jun-proteins plays a role in human papillomavirus-linked carcinogenesis in the genital tract (reviewed in zur Hausen, 1996) and increasing data are shedding light on the role of these proteins in the life cycle of mainly the mucosal HPV types in differentiating keratinocytes (Longworth and Laimins, 2004). The HPV types associated with cutaneous lesions react diversely in response to external or cellular factors (de Villiers et al, 1999;Ruhland and de Villiers, 2001). The expression of c-Jun and JunB is enhanced under the expression of bovine papillomavirus in mouse dermal fibroblasts leading to the formation of fibromatosis (Bossy-Wetzel et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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TAp63α indirectly regulates a cutaneous HPV promoter through complex formation with Jun family members

et al. 2006

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Human papillomaviruses in non-melanoma skin cancer

Cited by 47 publications

References 90 publications

RETRACTED ARTICLE: Human papillomavirus type 77 E6 protein selectively inhibits p53-dependent transcription of proapoptotic genes following UV-B irradiation

RETRACTED ARTICLE: Human papillomavirus type 77 E6 protein selectively inhibits p53-dependent transcription of proapoptotic genes following UV-B irradiation

Familial clustering of cancer at human papillomavirus‐associated sites according to the Swedish Family‐Cancer Database

TAp63α indirectly regulates a cutaneous HPV promoter through complex formation with Jun family members

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