Abstract
Human papilloma virus (HPV)-associated head and neck carcinoma is quite heterogeneous and most of the tumors arise in the oral cavity, oropharynx, hypopharynx and larynx. HPV was just recently recognized as an emerging risk factor for oropharyngeal squamous cell carcinoma (OSCC). HPV(+) tumors represent 5-20% of all head and neck squamous-cell carcinomas (HNSCCs) and 40-90% of those arising from the oropharynx, with widely variable rates depending on the geographic area, population, relative prevalence of environment-related SCC and detection assay. Different carcinogenic mechanisms are most likely implicated in cervical and oropharyngeal carcinogenesis. The most certain carcinogenic genotype for the head and neck region and the most common high-risk HPV genotype, HPV-16, is frequently detected in OSCC. A combination of p16INK4A expression and molecular detection of HPV DNA is the gold standard for the viral identification in tissue and exfoliated cell samples. Differences in the biology of HPV(+) and HPV(-) OSCC may have implications for the management of patients. New immunotherapy drugs based on the release of the co-inhibitory receptors, cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and programmed-death 1 (PD-1) have currently emerged. The goal of therapeutic cancer vaccination is inculcation of a persistent, tumor antigen-specific T cell response which kills tumor cells. The efficacy of the current HPV vaccines, Cervarix and Gardasil, in preventing HPV-related HNSCC is at present unknown. Treatment de-escalation is recommended as the current management of HPV-induced HNSCCs.
Highlights
Human papilloma virus (HPV) infections are mainly sexually transmitted through direct skin or mucosa contact and represent the most common sexually transmitted infections worldwide
HPV-16 accounts for approximately 50% of cervical carcinomas and more than 90% of HPV(+) carcinomas of the oropharynx
Exposure to HPV is determined by well known risk factors for most sexually transmitted infections, while determinants of susceptibility and infectivity are much less established [12]
Summary
Head and neck carcinomas (HNCs) is the sixth most common cancer with an annual incidence of ~400.000 cases [15] and represents about 3.5% of all malignant tumors in the western societies [16, 17] and other parts of the world. HPV involvement in head and neck carcinogenesis was initially reported 30 years ago [10, 11]; it was just recently recognized as an emerging risk factor for oropharyngeal squamous cell carcinoma (OSCC) [19]. Among the other extra-oropharyngeal subsites, HPV might have a role in the supraglottic larynx [27], whose marginal region is contiguous with the oropharynx, and it may account for the high-risk HPV infection rate reported in laryngeal SCCs [28, 29]. HPV detection rates, including high risk HPV viral load, were found to be significantly higher in tonsillar cancers than in other head and neck carcinomas [31, 32]. Recent data in oral cancers indicate that p16INK4A over-expression is due to different mechanisms and high-risk HPV infection is very rarely detectable in oral SCCs [27, 35]. HPV(+) OSCCs belong to a distinct clinical and molecular entity with a looser association with tobacco and alcohol
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