Papillomavirus DNA in Basal Cell Carcinomas of Immunocompetent Patients: an Accidental Association?

Wieland, Ulrike; Ritzkowsky, Andreas; Stoltidis, Marius; Weissenborn, Soenke J.; Stark, Sabine; Ploner, Miriam; Majewski, Sławomir; Jabłońska, Stefania; Pfister, Herbert; Fuchs, Pawel G.

doi:10.1046/j.1523-1747.2000.00015.x

Cited by 86 publications

(91 citation statements)

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“…19,21 The greatest difference was found for patients diagnosed with BCC, where we only detected HPV38 or HPV38b[FA125] in two of 118 patients (1.7%), compared to previous reports with positivity rates ranging from 7% to as high as 55%. 19,21,23 This discrepancy is likely to be attributable to the removal of superficial cells with tape, which is known to reduce HPV DNA prevalences. 16 The virus DNA load was higher in the swab samples taken from the tops of the lesions than in the corresponding biopsies, indicating that most of the HPV38 DNA was present on top of the lesions and only to a minor extent in the lesions themselves.…”

Section: Discussionmentioning

confidence: 99%

“…19,20 HPV38 has been proposed to be a skin cancer-associated HPV type based on reported prevalences of 7-55% in BCC, 13-46% in SCC and 17-43% in actinic keratosis (AK). 19,[21][22][23] In comparison, HPV38 has been detected in 10% of healthy skin biopsies 19 and in 25% of plucked eyebrow hairs. 24 A possible reason for the variability in reported HPV DNA prevalences is the fact that the skin surface contains high amounts of viral DNA, whereas the skin lesions themselves contain less viral DNA.…”

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confidence: 99%

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Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Hazard

Eliasson

Dillner

et al. 2006

Intl Journal of Cancer

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The human papillomaviruses (HPVs) exist as more than 100 distinct types. While variants of HPV are common, only few HPV subtypes have been reported. HPV type 38 has been proposed to be associated with nonmelanoma skin cancer (NMSC), with reported prevalences of up to 55%. A subtype of HPV38 was cloned, completely sequenced and found to have a 96% sequence similarity to prototype HPV38 in the L1 open reading frame. The presence of prototype HPV38 and HPV38b[FA125] was examined in paired biopsies of tape-stripped skin lesions and healthy skin from 269 immunocompetent patients by real-time PCR. Prototype HPV38 and HPV38b[FA125] were present in seven (3%) and five (2%) lesions, respectively, in viral loads ranging from one copy per 150 cells to one copy per 70,000 cells. In summary, we found that HPV38 is heterogeneous and is one of so far only few HPVs that contain subtypes. The heterogeneity needs to be considered in studies of the biology of this virus. ' 2006 Wiley-Liss, Inc.Key words: HPV; subtype; nonmelanoma skin cancer; multiplyprimed rolling circle amplification Nonmelanoma skin cancers (NMSC) are the most prevalent malignancies in the Caucasian population 1 and an increase in prevalence has been seen in European countries during the last few years. 2 NMSC comprises basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). BCC has a relatively good prognosis, while SCC accounts for up to 20% of all deaths from skin cancer. 3 NMSC are often found on sun-exposed sites in patients with the rare inherited genetic disease epidermodysplasia verruciformis (EV). 4 These patients are highly susceptible to human papillomavirus (HPV) infections 5,6 mainly by the Beta-papillomaviruses, a phylogenetic subgroup of cutaneous HPVs (e.g., HPV5 and HPV8). 7 These HPV types are detectable in skin carcinomas, as well as in control specimens of healthy skin from the general population. [8][9][10][11][12] There are more than 100 different HPV types that have been completely sequenced. 7 In addition, there appears to exist about 100 additional putative HPV types, with sequence information so far available only from PCR amplimers. 8,[13][14][15][16] Variants of HPV types contain more than 98% sequence homology in the L1 open reading frame (ORF). 7 Variants is a common finding that appears to associate with ethnic groups and sometimes even with biologic behavior of the virus. 17,18 By contrast, subtypes containing 90-98% sequence homology in the L1 region are very rare, with HPV 68a/HPV68b, HPV46, HPV55 and HPV64 (now known to be subtypes, originally thought to be different viruses) being the only fully characterized examples. 7,17 Although the reasons for this are not known, existence of subtypes has profound implications for design of virus detection systems and for understanding of the biology of the viruses.Epidemiological studies have established a causal association between UV-radiation and NMSC, 3 but the role of HPV in these cancers remains to be elucidated.A recent study 19 has demonstrated that the early proteins E...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Hazard

Eliasson

Dillner

et al. 2006

Intl Journal of Cancer

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“…Broad-spectrum A6/A8-PCR was performed as previously described. 23 Biotinylated internal PCR products (about 270 bp) were employed in the same bead-based multiplex hybridization assay mentioned above for HPV typing. 20,24 SPF10-PCR and reverse line blot hybridization of biotinylated 65 bp PCR products were performed according to the manufacturer's instructions (INNO-LiPA HPV Genotyping Extra assay, Innogenetics, Gent, Belgium).…”

Section: Cancer Cell Biologymentioning

confidence: 99%

Human papillomavirus DNA load and p16^INK4aexpression predict for local control in patients with anal squamous cell carcinoma treated with chemoradiotherapy

et al. 2014

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As the detection rate of HPV-DNA in anal carcinoma commonly exceeds 90%, a comparison between sole HPV-positive and HPV-negative cancers with respect to treatment response following chemoradiotherapy (CRT) and long-term oncological outcome is challenging. Against this background, we aimed to assess HPV types and HPV DNA load in formalin-fixed paraffinembedded tissue (FFPE) of 95 patients treated with standard CRT for anal cancer to correlate viral load ( /> median) with local failure, distant metastases, cancer-specific (CSS) and overall survival (OS) rates. Various clinicopathologic parameters and the immunohistochemical marker p16 INK4a were evaluated for any correlation with HPV16 DNA load and were included in uni-and multivariate analyses. The overall prevalence of HPV DNA was 95.8% with HPV16 monoinfection being the most commonly encountered HPV type (78.9%), followed by HPV16 and 31,35,39,44, 58, 66 and 81 dual infection in 9 patients (9.5%). HPV16 DNA load was significantly associated with p16 INK4a expression (p 5 0.001). Patients with HPV16 DNA load median and low p16 INK4a expression showed significantly worse local control (HPV16 DNA load: univariate p 5 0.023, multivariate p 5 0.042; p16 INK4a : univariate p 5 0.021), and OS (HPV16 DNA load: univariate p 5 0.02, multivariate p 5 0.03). Moreover, a combined HPV16 DNA load and p16 INK4a variable revealed a significant correlation to decreased local failure, and increased CSS and OS (p 5 0.019, p 5 0.04 and p 5 0.031). In conclusion, these data indicate that HPV16 DNA load and p16 INK4a expression are significant prognostic factors for local tumor control and overall survival of patients with anal SCC following CRT.The majority of anal squamous cell carcinoma (SCC) is considered to originate from infection with human papilloma viruses (HPV). 1,2 Especially the role of high-risk oncogenic HPV types, most prominently HPV type 16 (HPV16), in the etiology of anal SCC is well established by a multitude of epidemiological and experimental investigations. 3,4 As a consequence, technologies for the detection of HPV DNA may constitute valuable screening tools for anal malignancies and are of important clinical relevance, especially after the development of a preventive vaccine for both men and women. 5 Depending on the method used, the prevalence of HPV DNA in anal carcinoma ranges from 75% to 100% with HPV16 (>75%) and less frequent HPV18 (<10%) detection in the majority of cases. 6,7 In clinical series of head and neck as well as cervical SCC, recent data indicate that treatment response to radiotherapy (RT) or chemoradiotherapy (CRT) is superior in HPV-positive tumors as compared with their HPV-negative counterparts. [8][9][10] An increased sensitivity of HPV-positive tumor cells towards irradiation and chemotherapeutic agents was also observed in vitro and in animal studies. [11][12][13] However, as the detection rate of HPV DNA in anal SCC commonly exceeds 90%, a comparison between sole HPV-positive and HPV-negative cancers with respect to treatment respon...

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“…40 PCR products (5 ll) were separated on 2% agarose gels and visualized by ethidium bromide staining. For HPV typing biotinylated A6/A8-PCR products were hybridized with 37 type-specific digoxigenin-labeled oligonucleotide probes in an enzyme-immunoassay (EIA) as previously described.…”

Section: Ink4amentioning

confidence: 99%

Marked differences in survival rate between smokers and nonsmokers with HPV 16‐associated tonsillar carcinomas

Hafkamp

Manni

Haesevoets

et al. 2008

Intl Journal of Cancer

308

293

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Oncogenic human papillomavirus (HPV) is a causative agent in a subgroup of head and neck carcinomas, particularly tonsillar squamous cell carcinomas (TSCC). This study was undertaken because controversial data exist on the physical status of HPV-DNA and the use of p16INK4A overexpression as surrogate HPV marker, and to examine the impact of HPV and tobacco consumption on the clinical course of TSCC. Tissue sections of 81 TSCC were analyzed by HPV 16-specific fluorescence in situ hybridization (FISH) Head and neck squamous cell carcinomas (HNSCC) account for 4% of all malignancies in the Western world, for up to 50% of all malignancies in Southeast Asian countries and for 6.5% of all annual cancer cases worldwide.1 HNSCC is associated with severe disease-and treatment-related morbidity and because treatment has not improved greatly in recent years, the 5-year survival rate remains 50%. HNSCC develop in various anatomical defined regions, including the oral cavity, larynx and pharynx. These organ-specific tumors each show specific clinical presentations and outcome, and are treated by different strategies. 2,3 The median age at presentation is 60 years and approximately two-third of patients are male. Well-known risk factors in the etiology of HNSCC are cigarette smoking combined with alcohol consumption in Western countries, or with betel quid chewing in Asia. A history of tobacco use is present in 90% of patients who develop oral cavity cancers. 2,3Despite these evident associations, the exact mechanisms by which these factors cause tumor initiation and progression are not fully understood. Furthermore, the fact that most tobacco and alcohol users do not develop HNSCC and that in recent years more often individuals without a history of these traditional risk factors have been witnessed, 4 underlines the complexity of HNSCC pathogenesis and a role for additional factors in the disease process.Increasing evidence suggests that human oncogenic papillomaviruses (HPVs), known to cause uterine cervical and other anogenital cancers, may also be of importance in the pathogenesis of HNSCC. 5 The strongest association has been found for oropharyngeal carcinomas, especially tonsillar carcinomas.6-11 Sero-positive patients for HPV 16 or with a history of HPV-related anogenital cancer also show increased risk rates of developing oropharyngeal cancer.12,13 The prevalence of HPV-exhibiting HNSCC, however, varies broadly amongst several studies (2-76%) due to differences in the population, combination of histological subsites, type and number of specimens analyzed, and detection methods used. 7,14 Thus, besides determining the presence of HPV DNA it has been suggested to better define the biological association of oncogenic HPV with these tumors, e.g., by means of assessing the viral copy number per cell, the viral oncoprotein E6/E7 expression levels, perturbation of pRb-dependent cell cycle control, or the physical status of the virus (episomal or integrated). 15 In this way, several reports have shown that HPV 16 is predomi...

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Papillomavirus DNA in Basal Cell Carcinomas of Immunocompetent Patients: an Accidental Association?

Cited by 86 publications

References 29 publications

Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Human papillomavirus DNA load and p16^INK4aexpression predict for local control in patients with anal squamous cell carcinoma treated with chemoradiotherapy

Marked differences in survival rate between smokers and nonsmokers with HPV 16‐associated tonsillar carcinomas

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Papillomavirus DNA in Basal Cell Carcinomas of Immunocompetent Patients: an Accidental Association?

Cited by 86 publications

References 29 publications

Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Subtype HPV38b[FA125] demonstrates heterogeneity of human papillomavirus type 38

Human papillomavirus DNA load and p16INK4aexpression predict for local control in patients with anal squamous cell carcinoma treated with chemoradiotherapy

Marked differences in survival rate between smokers and nonsmokers with HPV 16‐associated tonsillar carcinomas

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Human papillomavirus DNA load and p16^INK4aexpression predict for local control in patients with anal squamous cell carcinoma treated with chemoradiotherapy