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Evidence of the causal role of human papillomavirus type 58 in an oropharyngeal carcinoma

Lorena Baboci123, Paolo Boscolo-Rizzo4, Dana Holzinger1, Roberta Bertorelle3, Lorena Biasini3, Angelika Michel1, Markus Schmitt1, Giacomo Spinato5, Rossana Bussani6, Laia Alemany7, Giancarlo Tirelli5, Maria Cristina Da Mosto4, Annarosa Del Mistro3* and Michael Pawlita1

Author Affiliations

1 Division of Genome Modifications and Carcinogenesis (F020), Research Program Infection and German Cancer Research Center (DKFZ), ImNeuenheimer Feld 280, Heidelberg 69120, Germany

2 Department of Surgery, Oncology and Gastroenterology, Immunology and Oncology Section, University of Padua, Via Gattamelata, 64, Padua 35128-I, Italy

3 Veneto Institute of Oncology IOV - IRCCS, Immunology and Molecular Oncology Unit, Via Gattamelata, 64, Padua 35128-I, Italy

4 Department of Neurosciences, ENT Clinic and Regional Center for Head and Neck Cancer, University of Padua, School of Medicine, Treviso Regional Hospital, Piazzale Ospedale 1, Treviso 31100, Italy

5 Head and Neck Department, Hospital of Cattinara, University of Trieste, Strada di Fiume 447, Trieste 34149, Italy

6 Pathology Department, Hospital of Cattinara, University of Trieste, Strada di Fiume 447, Trieste 34149, Italy

7 IDIBELL, Institut Catalàd’ Oncologia - Catalan Institute of Oncology, Avda Gran Via de l’Hospitalet, Barcelona 199-203, Spain

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Virology Journal 2013, 10:334  doi:10.1186/1743-422X-10-334

Published: 12 November 2013


Persistent human papillomavirus infection (HPV) is recognized as an important etiologic factor for a subset of head and neck squamous cell carcinomas (SCC), especially those arising from the oropharynx. Whereas HPV16 accounts for the majority of HPV DNA-positive oropharyngeal SCC, infections with other mucosal high-risk HPV types are quite rare and biological data demonstrating their causal involvement are insufficient. Here we present the first case of an oropharyngeal SCC driven by HPV type 58. A 69-year-old Caucasian woman presented with an enlarged and firm left tonsil. A computed tomography scan showed a left tonsillar mass, extending to the soft palate and the glossotonsillar sulcus. The patient underwent extended radical tonsillectomy and ipsilateral selective neck dissection. Pathology confirmed an infiltrating, poorly differentiated SCC of the left tonsil with node metastasis (pT2N1). Adjuvant external beam radiation therapy (60 Grays (Gy)) was administered. After 1 year of follow-up, the patient is well with no evidence of cancer recurrence. HPV analyses of the tumor tissue by BSGP5+/6+ −PCR/MPG, targeting 51 mucosal HPV types, showed single positivity for HPV type 58. Presence of HPV58 E6*I RNA demonstrated biological activity of the virus in the tumor tissue, and presence of serum antibodies to HPV58 oncoproteins E6 and E7 indicated presence of an HPV58-driven cancer. Overexpression of cellular protein p16INK4a and reduced expression of pRb, two cellular markers for HPV-induced cell transformation, were observed. Exons 4–10 of TP53 showed no mutations or polymorphisms. The presence of HPV58 as single HPV infection in combination with a broad variety of direct and indirect markers of HPV transformation provides comprehensive evidence that this oropharyngeal SCC was driven by HPV58.

HPV58; Head and neck squamous cell carcinoma; HPV carcinogenesis; HPV E6 and E7; HPV antibody; p16INK4a; pRb; p53