- 3/11/2005
- S Syrjanen
- J Clin Virol, March 1, 2005; 32 Suppl: 59-66
The term “head and neck cancer” has been widely adopted in the recent literature, to include the lesions at several anatomic sites: the lip, oral cavity, nose and para-nasal sinuses, naso-pharynx, oro-pharynx, hypo-pharynx, and larynx. In this report, the data on human papillomavirus (HPV) involvement in oral, oro-pharyngeal, sino-nasal, and laryngeal carcinomas are reviewed.
Our group was the first to present evidence on the involvement of HPV infections in both laryngeal and oral carcinogenesis, prompted by the discovery of morphological similarities between oral and cervical squamous cell lesions. The latest meta-analyses of the epidemiological studies as well as the multi-centre case-control studies have confirmed HPV as an independent risk factor for oral cancer, with a range of odds ratios (OR) between 3.7 and 5.4.
Until 2002, 4768 oral carcinomas have been analysed for HPV DNA, and 22% were reported to contain HPV by any of the detection techniques. Of all non-genital cancers, tonsillar carcinomas appear to have the highest prevalence of HPV. By the end of 2002, 422 cases of tonsillar carcinoma have been analyzed for the presence of HPV DNA, with the overall detection rate of 51%. HPV 16 is the most prevalent HPV type found in 84% of HPV DNA-positive tumours. HPV seems to be mainly episomal in tonsillar carcinomas, but the significance of this observation is still obscure.
Interestingly, patients with HPV 16-positive tumours seem to have a better overall- and disease-specific survival, as compared with the HPV-negative group. To date, 1041 sino-nasal papillomas have been analysed for HPV and 347 (33%) cases have been positive, whereas of the 322 sino-nasal carcinomas analysed so far, 70 (22%) have been positive for any HPV type.
Laryngeal squamous cell papilloma and recurrent respiratory papillomatosis (RRP) are well-established HPV-induced tumours, whereas the role of HPV in laryngeal carcinomatosis remains controversial. The molecular mechanisms of HPV-associated carcinogenesis of the head and neck require further study.
Author’s affiliation:
Department of Oral Pathology, Institute of Dentistry, Faculty of Medicine, University of Turku, Lemminkäisenkatu 2, FIN-20520 Turku, Finland
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