Prevailing papillomavirus types in non-melanoma carcinomas of the skin in renal allograft recipients

Villiers, Ethel‐Michele de; Lavergne, Donna; McLaren, K M; Benton, E. C.

doi:10.1002/(sici)1097-0215(19971104)73:3<356::aid-ijc9>3.0.co;2-z

Cited by 202 publications

(99 citation statements)

References 25 publications

(36 reference statements)

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“…It is well known that human papilloma virus (HPV), which inactivates p53 and Rb, is involved in the development of cervical squamous carcinoma and the Rb-inactivation probably contributes to the high p16 INK4a expression in cervical cancer. [21][22][23] The role of HPV in NMSC has been debated and extensively studied but remains elusive. 22 The similarities between squamous cell carcinomas of the skin and cervix are, nevertheless, profound and both the Rb-inactivation and high p16 INK4a expression support a common and probably HPV-associated etiology.…”

Section: Discussionmentioning

confidence: 99%

Retinoblastoma protein function and p16INK4a expression in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma of the skin and links between p16INK4a expression and infiltrative behavior

2004

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p16 INK4a is involved in many important regulatory events in the cell and the expression and function is closely associated with the retinoblastoma protein (Rb). Earlier, we have in colorectal cancer and in basal cell carcinoma showed that p16 INK4a is upregulated at the invasive front causing cell cycle arrest in infiltrative tumor cells via a functional Rb. This role for p16 INK4a as a regulator of proliferation when tumor cells infiltrate might besides a general cyclin-dependent kinase (cdk) inhibitory effect explain why p16 INK4a is deregulated in many tumor forms. The expression pattern of p16 INK4a in relation to Rb-function in squamous cancer and precancerous forms of the skin has not been fully detailed. We therefore characterized the expression of p16 INK4a , Rb-phosphorylation and proliferation in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma with special reference to infiltrative behavior. The expression of p16 INK4a varied between the lesions, with weak and cytoplasmic p16 INK4a expression and functional Rb in actinic keratosis. Strong nuclear and cytoplasmic p16 INK4a expression was observed in all carcinomas in situ in parallel with lack of Rb-phosphorylation but high proliferation indicating a nonfunctional Rb. Invasive squamous carcinoma showed a mixed p16 INK4a expression pattern where some tumors had strong cytoplasmic p16 INK4a expression, large fraction of Rb-phosphorylated cells and high proliferation. Interestingly, despite this disability of p16 INK4a to inhibit proliferation there was an upregulation of cytoplasmic p16 INK4a in infiltrative cells compared to tumor cells towards the tumor center. A similar scenario but strong and combined nuclear and cytoplasmic p16 INK4a expression in infiltrative cells, was observed in other invasive squamous cancers. This suggests that the p16 INK4a upregulation in infiltrative cells is governed independently of the subcellular localization or of the potential to affect proliferation via Rb, and suggests a potentially proliferation independent function for p16 INK4a in infiltrative behavior.

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Section: Discussionmentioning

confidence: 99%

Retinoblastoma protein function and p16INK4a expression in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma of the skin and links between p16INK4a expression and infiltrative behavior

2004

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“…HPV-5, -8, -9, -12, -14, -15, -17 and -19-25 (Kremsdorf et al, 1984;Orth et al, 1978), has been found in these patients. Some skin HPV types, mainly HPV-5 and HPV-8, have been found in skin cancer lesions, for example in EV patients (Jablonska & Majewski, 1994, Orth et al, 1979 and in immunosuppressed patients (Bens et al, 1998;Berkhout et al, 2000;de Villiers et al, 1997), and have therefore been suggested to be high-risk HPVs for these patients. However, in recent years it has been found that skin HPV types are widely spread among humans, giving rise to subclinical infections generally without causing warts or other lesions (Antonsson et al, 2000;Astori et al, 1998;Boxman et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Prevalence and type spectrum of human papillomaviruses in healthy skin samples collected in three continents

Antonsson

Erfurt

Hazard

et al. 2003

Journal of General Virology

165

149

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In order to investigate whether previous findings of ubiquitous skin papillomavirus infection in Caucasians apply to populations from other parts of the world, skin swab samples from Bangladesh, Japan, Ethiopia and Zambia were analysed in parallel with Swedish samples. The prevalence of HPV DNA in the material from Bangladesh was 68 %, Japan 54 %, Ethiopia 52 %, Zambia 42 % and Sweden 70 %. A great multiplicity of genotypes was demonstrated by the finding of 88 HPV types or putative types in 142 HPV DNA-positive samples in total. Double or multiple genotypes were frequently found in the same sample. The most prevalent HPV type was HPV-5, with an overall prevalence of 6?5 %. This was also the only type that was found in samples from all of the countries in the study. The results presented show that commensal skin HPV infections have a worldwide distribution with a very broad spectrum of genotypes.

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“…The human papillomavirus (HPV) family is ubiquitous in the human population and more than 100 virus types have been identi®ed (de Villiers et al, 1997). The viruses are small double-stranded DNA viruses with a genome of approximately 8 kb.…”

Section: Introductionmentioning

confidence: 99%

The role of the E6-p53 interaction in the molecular pathogenesis of HPV

1999

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Human papillomaviruses (HPVs) are associated with a number of clinical conditions, of which the most serious is cervical carcinoma. The E6 protein of the oncogenic, mucosal-speci®c HPV types has been shown to complex with p53 and, as a result, target it for rapid proteasomemediated degradation. As a consequence, p53's growtharrest and apoptosis-inducing activities are abrogated. Since p53 is frequently wild type in cervical cancers, unlike other cancers in which it is often mutated, the notion has arisen that E6's activity with respect to p53 is equivalent to an inactivating mutation of p53. In addition, several studies have shown that the pathways both upstream and downstream of p53 are intact in cervical cancers; this suggests the potential importance of the E6 ± p53 interaction for therapeutic intervention. However, like all viral oncoproteins, E6 is a multifunctional protein and a plethora of other cellular targets has been identi®ed. Indeed, E6's interactions with some of these additional targets appear to be equally important in the pathogenesis of HPV, and may also represent valid targets for therapeutic intervention.

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Prevailing papillomavirus types in non-melanoma carcinomas of the skin in renal allograft recipients

Cited by 202 publications

References 25 publications

Retinoblastoma protein function and p16INK4a expression in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma of the skin and links between p16INK4a expression and infiltrative behavior

Retinoblastoma protein function and p16INK4a expression in actinic keratosis, squamous cell carcinoma in situ and invasive squamous cell carcinoma of the skin and links between p16INK4a expression and infiltrative behavior

Prevalence and type spectrum of human papillomaviruses in healthy skin samples collected in three continents

The role of the E6-p53 interaction in the molecular pathogenesis of HPV

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