[Comment] Endpoints in human papillomavirus-related oropharyngeal cancer trials

Between 1995 and 2005, our understanding of the demographics of head and neck cancer underwent a dramatic change. It became evident that most oropharyngeal carcinomas were driven by high-risk human papillomavirus (HPV) infection as opposed to p53 or p16 mutations in environmentally caused cancers.1 Furthermore, patients with HPV-associated malignancy had substantially better clinical outcomes because of the sensitivity of their tumours to chemotherapy and radiation compared with the therapy resistance seen in those cancers caused by environmental carcinogens.