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Over recent years, human papillomavirus (HPV) has been shown to be a major risk factor for head and neck squamous cell cancer (HNSCC), and particularly oropharyngeal squamous cell carcinoma.1 ,2 In 2007, the International Agency for Research on Cancer recognised HPV as a carcinogen associated with malignant transformation in this subset of head and neck cancers. It is now well established that HPV-induced oropharyngeal cancers and those caused by other factors (such as smoking and alcohol abuse—a combination of heavy smoking and drinking leads to an almost 50-fold increased risk of oral and pharyngeal cancer3) are two separate entities, with distinct aetiologies, clinical characteristics, prognoses and a different epidemiology and molecular basis.4
The incidence of HPV-associated HNSCC has risen rapidly in the Western world over the past 40 years.5–8 For example, there has been an estimated threefold increase in tonsillar cancer during this period,9 and the overall estimated population-level incidence of HPV-positive oropharyngeal cancer, which was 2.6 per 100 000 in the USA in 2004,6 is set to triple again in the next 20 years.10 Interestingly, the overall incidence of HNSCC is falling at a time when the incidence of HPV-induced cancer has risen, with the result that the proportion of HPV-positive tonsillar cases has risen from <25% in the 1970s to 93% of cases by 2007 in parts of the developed world.7 …