Detection and typing of human papillomaviruses in mucosal and cutaneous biopsies from immunosuppressed and immunocompetent patients and patients with epidermodysplasia verruciformis: a unified diagnostic approach

Surentheran, T.; Harwood, Catherine A.; Spink, Patricia J.; Sinclair, Alasdair; Leigh, Irene M.; Proby, Charlotte M.; McGregor, Jane; Breuer, Judith

doi:10.1136/jcp.51.8.606

Cited by 40 publications

(43 citation statements)

References 16 publications

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“…The cancers in EV individuals predominantly occur at body sites exposed to sunlight, pointing to a role for ultra violet (UV) radiation in the development of the disease (Orth et al, 1979). In addition to EV, a role for HPVs has also been postulated in the development of non-melanoma skin cancers (NMSC) in both immunocompetent and immunocompromised individuals, such as organ transplant recipients (Jablonska, 1990;Purdie et al, 1993;de Jong-Tieben et al, 1995;Shamanin et al, 1996;Hop¯et al, 1997;Surentheran et al, 1998). Interestingly, these individuals also often develop NMSC at UV-exposed sites (reviewed in Proby et al, 1996).…”

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confidence: 99%

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

2000

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In addition to their role in anogenital cancer, human papillomaviruses (HPVs) are also involved in the development of a range of cutaneous lesions. HPV types 5 and 8 are associated with the development of skin cancers in individuals with Epidermodysplasia verruciformis (EV). A broad spectrum of HPV types are also commonly found in non-melanoma skin cancers in immunocompromised individuals, such as organ transplant recipients. The skin cancers in EV and immunocompromised patients occur predominantly at body sites exposed to ultra violet (UV) radiation, pointing to a key role for UV in their development. Here we show that the E6 protein from a range of cutaneous HPV types e ectively inhibits apoptosis in response to UV damage. This occurs in both p53 null and wild type cells and does not require p53 degradation. Oncogene (2000) 19, 592 ± 598.

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confidence: 99%

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

2000

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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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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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“…Shortly after the onset of immunosuppressive therapy, HPVinduced warts develop in these individuals, and 20 years after the beginning of immunosuppression nonmelanocytic skin cancer can be found in up to 70% of these patients (6). A similar situation has been described in the rare genetic disorder epidermodysplasia verruciformis, but the mechanisms leading to the development of skin cancer and especially the role of papillomaviruses are not yet fully understood (3,12,38). …”

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Identification of the E9^E2C cDNA and Functional Characterization of the Gene Product Reveal a New Repressor of Transcription and Replication in Cottontail Rabbit Papillomavirus

Jeckel

Loetzsch

Huber

et al. 2003

J Virol

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Cottontail rabbit papillomavirus (CRPV) genomes mutated in the trans-activation domain of the E2 protein, which stimulates both viral DNA replication and transcription, are severely impaired in their ability to induce tumors in New Zealand White rabbits. A number of papillomaviruses encode, in addition to full-length E2, a shortened E2 protein or an E2 protein fused to a short stretch of amino acids derived from the small E8 open reading frame that counteract the activities of E2. We identified and cloned the novel cDNA E9^E2C of CRPV from papillomas of New Zealand White and cottontail rabbits and characterized the functions of the encoded gene product. E9^E2C was shown to be a bona fide repressor of minimal viral promoters, with the E9 domain being essential for this activity, and to repress E1/E2-dependent replication of a CRPV origin construct. In addition, E9^E2C counteracted the transactivation effect of the full-length E2 on minimal promoters containing several E2 binding sites. To investigate the role of E9^E2C in tumorigenesis, we constructed two CRPV genomes mutated in E9^E2C. One, designated CRPV-E9atgmut-pLAII, contained a mutation in the unique start codon in the E9 open reading frame, and the second E9^E2C mutant was constructed by the introduction of a stop codon close to the splice donor site at nucleotide 3714 that additionally prevented the correct splicing of the transcript. When we infected New Zealand White rabbits with these constructs, we surprisingly noted no differences in tumor induction efficiency, viral genome copy number, and viral transcription in comparison to wild-type CRPV.Papillomaviruses have attracted special attention because persistent infection with a subset of human papillomaviruses (HPV) is a necessary factor for the development of anogenital cancer (4, 43). In contrast, the role of HPV in skin cancer, which is the most common cancer of the Caucasian race, is still undefined, although a very first link was obtained in 1935, when Rous et al. (30) described the development of squamous cell carcinomas in rabbits after experimental infection with cottontail rabbit papillomavirus (CRPV). Skin cancer in humans has been recognized as a common side effect in longterm immunosuppressed patients, who have a 65-fold increased risk compared to immunocompetent individuals. Shortly after the onset of immunosuppressive therapy, HPVinduced warts develop in these individuals, and 20 years after the beginning of immunosuppression nonmelanocytic skin cancer can be found in up to 70% of these patients (6). A similar situation has been described in the rare genetic disorder epidermodysplasia verruciformis, but the mechanisms leading to the development of skin cancer and especially the role of papillomaviruses are not yet fully understood (3,12,38).The only model system for studying tumor induction and progression after infection of the skin with papillomaviruses is the domestic rabbit infected with CRPV, in which local tumors develop within 3 to 6 weeks postinfection and progress within 6 to 1...

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Detection and typing of human papillomaviruses in mucosal and cutaneous biopsies from immunosuppressed and immunocompetent patients and patients with epidermodysplasia verruciformis: a unified diagnostic approach

Cited by 40 publications

References 16 publications

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

RETRACTED ARTICLE: E6 proteins from diverse cutaneous HPV types inhibit apoptosis in response to UV damage

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

Identification of the E9^E2C cDNA and Functional Characterization of the Gene Product Reveal a New Repressor of Transcription and Replication in Cottontail Rabbit Papillomavirus

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