Head and neck squamous cell carcinoma (HNSCC) develops in the mucosal linings of the upper aerodigestive tract and contributes to approximately 5% of all cancers in the Western world. Tumors develop either by exogenous carcinogen exposure (smoking, alcohol drinking) or human papillomavirus (HPV) infection. Particularly the squamous cell carcinomas in the oropharynx (OPSCC) encompass a high proportion of HPV-positive (HPV+ve) cases. The incidence of OPSCC is rising, which is attributed to HPV. Every year approximately 100,000 patients suffer from HPV-attributable OPSCC worldwide. HPV+ve and HPV-negative (HPV-ve) OPSCC are considered different disease entities. HPV+ve tumors have a much more favorable prognosis than HPV-ve tumors, and various risk models indicate that HPV status is the major predictor of prognosis in OPSCC. In 2004, it was shown for the first time that there are major genetic differences between HPV+ve and HPV-ve OPSCC. Subsequently a plethora of molecular studies revealed that besides major genetic differences, HPV+ve and HPV-ve OPSCC differ on the level of expression, microRNA profiles, and epigenetic profiles. In this presentation an overview of the molecular differences between HPV+ve and HPV-ve tumors will be presented, and the link to clinical behavior highlighted.
review
HPV+ve and HPV-negative (HPV-ve) OPSCC are considered different disease entities. HPV+ve tumors have a much more favorable prognosis than HPV-ve tumors, most likely as a consequence of major differences at the molecular level.