Abstract
Purposep16 overexpression was considered as surrogate marker to identify human papillomavirus (HPV)-associated oropharyngeal squamous cell carcinoma (OPSCCs).Methods102 patients with advanced stage OPSCCs treated primarily by transoral lasermicrosurgery were included. Prognostic associations of p16- and HPV-status were analyzed separately and combined.ResultsIn contrast to p16, the HPV-status resulted in no significant survival discrepancies (5-year overall survival (OS) HPV-positive 64.9%, HPV-negative 78.7%). Combining both markers, p16-positive (p16-positive/HPV-positive, p16-positive/HPV-negative) and p16-negative/HPV-negative groups demonstrated comparable high survival (OS 78.1% vs. 85.6% vs. 73.6%). Lowest survival was observed for patients with p16-negative/HPV-positive OPSCCs (OS 40.8%).Never smoking patients with p16-positive OPSCCs demonstrated the highest survival, whereas within former/current smokers with p16-positive and p16-negative disease it was comparable low (OS 90.0% vs. 63.0% vs. 57.4%).Conclusionsp16- and HPV-status should not be considered as equivalent markers for a better prognosis. Furthermore, they should not generally predominate patient associated factors like smoking.
Highlights
Oropharyngeal cancer constitutes 11.3% of all head and neck malignancies [1]
In the RTOG 1016 trial investigating radiotherapy combined with cetuximab or cisplatin in human papillomavirus (HPV)-positive oropharyngeal cancer patients, HPV-status was determined by p16-overexpression [17]
An algorithm of first p16-immunohistochemistry and for positive samples followed by HPV-DNA PCR was applied to define “HPV-positivity” [23, 38]. p16-overexpression is considered as a surrogate marker for oncogenic HPVinfection based on the high correlation found between both [16, 29]
Summary
Apart from the most prevalent risk factors of alcohol and tobacco consumption [2], a geographical divergent increasing subset of oropharyngeal squamous cell carcinomas (OPSCC) is characterized by human papillomavirus (HPV) infections [3,4,5,6,7,8]. Most commonly they are caused by the HPV-genotype 16 [9] while non-HPV16 HPV-genotypes were recognized with a high oncogenic potential [10].
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