Open Access Original research article

Does HPV type affect outcome in oropharyngeal cancer?

Anthony C Nichols12345*, Sandeep S Dhaliwal1, David A Palma234, John Basmaji1, Corina Chapeskie1, Samuel Dowthwaite1, Jason H Franklin124, Kevin Fung124, Keith Kwan5, Brett Wehrli5, Chris Howlett5, Iram Siddiqui5, Marina I Salvadori6, Eric Winquist24, Scott Ernst24, Sara Kuruvilla24, Nancy Read24, Varagur Venkatesan24, Biljana Todorovic27, J Alex Hammond24, James Koropatnick2347, Joe S Mymryk2347, John Yoo124 and John W Barrett1234

Author Affiliations

1 Department of Otolaryngology, Head & Neck Surgery, The University of Western Ontario, Room B3-431A, 800 Commissioners Road East, London, N6A 5W9, , Ontario, Canada

2 London Regional Cancer Program, London, Ontario, Canada

3 Lawson Health Research Institute, London, Ontario, Canada

4 Department of Oncology, The University of Western Ontario, London, Ontario, Canada

5 Department of Pathology, The University of Western Ontario, London, Ontario, Canada

6 Department of Paediatrics, Infectious Disease Division, The University of Western Ontario, London, Ontario, Canada

7 Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, Canada

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Journal of Otolaryngology - Head and Neck Surgery 2013, 42:9  doi:10.1186/1916-0216-42-9

Published: 1 February 2013

Abstract

Background

An epidemic of human papillomavirus (HPV)-related oropharyngeal squamous cell cancer (OPSCC) has been reported worldwide largely due to oral infection with HPV type-16, which is responsible for approximately 90% of HPV-positive cases. The purpose of this study was to determine the rate of HPV-positive oropharyngeal cancer in Southwestern Ontario, Canada.

Methods

A retrospective search identified ninety-five patients diagnosed with OPSCC. Pre-treatment biopsy specimens were tested for p16 expression using immunohistochemistry and for HPV-16, HPV-18 and other high-risk subtypes, including 31,33,35,39,45,51,52,56,58,59,67,68, by real-time qPCR.

Results

Fifty-nine tumours (62%) were positive for p16 expression and fifty (53%) were positive for known high-risk HPV types. Of the latter, 45 tumors (90%) were identified as HPV-16 positive, and five tumors (10%) were positive for other high-risk HPV types (HPV-18 (2), HPV-67 (2), HPV-33 (1)). HPV status by qPCR and p16 expression were extremely tightly correlated (p < 0.001, Fishers exact test). Patients with HPV-positive tumors had improved 3-year overall (OS) and disease-free survival (DFS) compared to patients with HPV-negative tumors (90% vs 65%, p = 0.001; and 85% vs 49%, p = 0.005; respectively). HPV-16 related OPSCC presented with cervical metastases more frequently than other high-risk HPV types (p = 0.005) and poorer disease-free survival was observed, although this was not statistically significant.

Conclusion

HPV-16 infection is responsible for a significant proportion of OPSCC in Southwestern Ontario. Other high-risk subtypes are responsible for a smaller subset of OPSCC that present less frequently with cervical metastases and may have a different prognosis.

Keywords:
Human papillomavirus; Oropharyngeal cancer; Epidemiology