Does HPV type affect outcome in oropharyngeal cancer? - PubMed (original) (raw)

doi: 10.1186/1916-0216-42-9.

Sandeep S Dhaliwal, David A Palma, John Basmaji, Corina Chapeskie, Samuel Dowthwaite, Jason H Franklin, Kevin Fung, Keith Kwan, Brett Wehrli, Chris Howlett, Iram Siddiqui, Marina I Salvadori, Eric Winquist, Scott Ernst, Sara Kuruvilla, Nancy Read, Varagur Venkatesan, Biljana Todorovic, J Alex Hammond, James Koropatnick, Joe S Mymryk, John Yoo, John W Barrett

Affiliations

Does HPV type affect outcome in oropharyngeal cancer?

Anthony C Nichols et al. J Otolaryngol Head Neck Surg. 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.

PubMed Disclaimer

Figures

Figure 1

Figure 1

Disease-free and overall survival by HPV status (A and B) and p16 status (C and D).

Figure 2

Figure 2

Disease-free (A) and overall survival (B) for HPV-positive patients stratified by HPV type.

References

    1. SEER Cancder Statistics Review, 1975–2008. Bethesda, MD: National Cancer Institute; 2011. http://seer.cancer.gov/csr/1975_2008/
    1. Marur S, D'Souza G, Westra WH, Forastiere AA. HPV-associated head and neck cancer: a virus-related cancer epidemic. Lancet Oncol. 2010;11(8):781–9. doi: 10.1016/S1470-2045(10)70017-6. - DOI - PMC - PubMed
    1. Chaturvedi AK, Engels EA, Pfeiffer RM. et al.Human papillomavirus and rising oropharyngeal cancer incidence in the United States. J Clin Oncol. 2011;29(32):4294–301. doi: 10.1200/JCO.2011.36.4596. - DOI - PMC - PubMed
    1. Nasman A, Attner P, Hammarstedt L. et al.Incidence of human papillomavirus (HPV) positive tonsillar carcinoma in Stockholm, Sweden: an epidemic of viral-induced carcinoma? Int J Cancer. 2009;125(2):362–6. doi: 10.1002/ijc.24339. - DOI - PubMed
    1. Ang KK, Harris J, Wheeler R. et al.Human papillomavirus and survival of patients with oropharyngeal cancer. N Engl J Med. 2010;363(1):24–35. doi: 10.1056/NEJMoa0912217. - DOI - PMC - PubMed

Publication types

MeSH terms

LinkOut - more resources