Novel ß-HPV49 Transgenic Mouse Model of Upper Digestive Tract Cancer

Viarisio, Daniele; Müller‐Decker, Karin; Zanna, Paola; Kloz, Ulrich; Aengeneyndt, Birgit; Accardi, Rosita; Flechtenmacher, Christa; Gissmann, Lutz; Tommasino, Massimo

doi:10.1158/0008-5472.can-16-0370

Cited by 32 publications

(35 citation statements)

References 29 publications

(38 reference statements)

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“…The other construction with HPV38 had no carcinogenic effect in the oral mucosa, in contrast to the skin, when UV light was used as a cofactor. These results highlight the important differences in the biological properties of certain β-papillomaviruses that seem to affect their oncogenic power in an anatomic site-specific manner [44, 45]. …”

Section: Hpv In Hnsccmentioning

confidence: 98%

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HPV in Head and Neck Carcinomas: Different HPV Profiles in Oropharyngeal Carcinomas – Why?

Syrjänen

2019

Acta Cytologica

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Background: The association of human papillomavirus (HPV) with head and neck squamous cell carcinoma (HNSCC) was first described in 1982–1983 by the authors of this review. Prompted by this discovery 35 years ago, an entirely new field of HPV research has emerged, resulting in a paradigm shift from smoking and alcohol as the only etiological factors to confirmation of HNSCC as an important group of HPV-related human malignancies. Summary: In this review, the authors first describe the scope (i.e., HNSCC) by the anatomic sites of the tumors. Their important site-specific differences in epidemiology are emphasized, and the misconceptions caused by the adopted practice of pooling all tumors from these divergent anatomic sites as a single entity (HNSCC) are pinpointed. The convincing evidence of the established risk factors (smoking and alcohol) is briefly addressed, before entering in the discussion on the causal role of HPV in HNSCC pathogenesis. The global HPV prevalence in different subsets of HNSCC is summarized using the data extracted from all meta-analyses published since 2010. Of all HNSCC subsets, oropharyngeal SCC has an HPV profile distinct form all the other subsets, and the possible mechanisms explaining this intimate association with HPV are discussed. Key Messages: Recent global trends show a constant increase in HNSCC rates particularly among younger age groups. The evidence on cigarette smoking and alcohol consumption as the prime risk factors of HNSCC is overwhelming. During the past 35 years, however, increasing evidence has accumulated implicating an important causal role of HPV in HNSCC. These data have important clinical implications, HPV detection and tailored treatment strategies for HPV-positive HNSCCs currently being an integral part of the oncological management practices of HNSCC.

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Section: Hpv In Hnsccmentioning

confidence: 98%

“…Cutaneous HPVs (β-papillomaviruses) might also have an impact on oral carcinogenesis [45]. HPV49 E6/E7-tg mice were highly susceptible to upper digestive tract carcinogenesis upon initiation with 4NQO to the same extent as the HPV16 E6/E7-tg mice.…”

Section: Hpv In Hnsccmentioning

confidence: 99%

HPV in Head and Neck Carcinomas: Different HPV Profiles in Oropharyngeal Carcinomas – Why?

Syrjänen

2019

Acta Cytologica

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“…In the presence of the chemical carcinogen, 4‐nitroquinoline 1‐oxide (4NQO), HPV‐16 E6 and E7 transgenic mice developed oral and esophageal carcinoma, but also benign papillomas. Recently, it was shown that the cutaneous HPVs ( Betapapillomaviruses ) can also have an impact on oral carcinogenesis . After treatment with 4NQO, HPV‐49 E6/E7‐Tg mice were highly susceptible to upper digestive tract carcinogenesis, upon initiation with 4NQO, to the same extent as HPV‐16 E6/E7‐Tg mice, whereas no effect was seen in HPV‐38 E6/E7‐Tg mice .…”

Section: Hpv Carcinogenesismentioning

confidence: 99%

Oral manifestations of human papillomavirus infections

Syrjänen

2018

European J Oral Sciences

112

144

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Papillomaviruses are one of the oldest viruses known, dating back 330 million years. During this long evolution, human papillomaviruses (HPV) have developed into hijackers of human cellular and immune systems in which they replicate and remain silent. Systematic studies on oral HPV infections and their outcomes are still scarce. Oral HPV infections have been linked to sexual behaviour, but recent evidence supports their horizontal, mouth‐to‐mouth, transmission. Most HPV infections in infants are acquired vertically from the mother during the intrauterine period, during delivery, or later via saliva. The best‐known benign clinical manifestations of HPV infection are oral papilloma/condyloma and focal epithelial hyperplasia. Evidence is emerging which suggests that some oral HPV infections might persist. Persistent HPV infection is mandatory for HPV‐associated malignant transformation. However, progression of HPV‐induced lesions to malignancy requires additional cofactors. In the early 1980s, we provided the first evidence that a subset of oral cancers and other head and neck cancers might be causally linked to HPV infection. This review summarizes current knowledge on the virus itself, its transmission modes, as well as the full spectrum of oral HPV infections – from asymptomatic infections to benign, potentially malignant oral lesions, and squamous cell carcinoma.

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“…However, in recent studies, HPV5, HPV 122, and gamma-11-and gamma-12-HPV have been found signifi cantly associated with head and neck tumours [40,14]. Additionally, Viarisio et al [41] have highlighted some functional similarities between mucosal HR HPV types such as HPV16 and beta-3 HPV49. Beta-3 HPV types appear to be more abundant in the nasal cavity than on the skin.…”

Section: Discussionmentioning

confidence: 99%

Mucosal and skin HPV types in tumour-free tonsils and tonsillar tumours

Saláková¹,

Koslabova²,

Grega³

et al. 2018

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Human papillomavirus (HPV) infection is associated with tonsillar cancer (TC) whose incidence in humans is increasing. Tonsillar tumours are not ordinarily preceded by clinically apparent precancerous lesions, and no markers of the early stage disease are available. Therefore, we evaluated the presence of an active HPV infection also in tumour-free tonsillar tissue. Formalin-fixed paraffin-embedded (FFPE) tonsillar specimens from 114 patients with TC and 114 age and gender matched controls were screened for the presence of HPV DNA, expression of HR-HPV E6 mRNA, and p16 overexpression. HPV DNA was identified in 3.5% of tumour-free tissues, HR-HPV16 and 58 and LR-HPV111 and 17 were each detected in a single sample. No HR HPV E6 mRNA and p16 overexpression was found. The prevalence of HPV DNA in TC was 69.3%, with HPV16 being the most common (94.9%). Eighty-four percent of HPV16-positive tumours expressed HR HPV E6 mRNA, while no E6 mRNA was present in samples positive for HPV52 and 58. The overexpression of p16 correlated well with HPV DNA in TC, but in tumour-free tonsils no overexpression of p16 was detected.Our data provide further evidence of the etiological role of HPV16 in TC. In tumour-free tissue, the presence of HR-HPVs was rare and silent, as shown by direct and indirect markers.

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Novel ß-HPV49 Transgenic Mouse Model of Upper Digestive Tract Cancer

Cited by 32 publications

References 29 publications

HPV in Head and Neck Carcinomas: Different HPV Profiles in Oropharyngeal Carcinomas – Why?

HPV in Head and Neck Carcinomas: Different HPV Profiles in Oropharyngeal Carcinomas – Why?

Oral manifestations of human papillomavirus infections

Mucosal and skin HPV types in tumour-free tonsils and tonsillar tumours

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