Prevalence of Human Papillomavirus in 45 Greek Patients with Oral Cancer

The relation between HPV and head and neck cancer has recently and extensively been investigated. The purpose of this study was to indentify HPV genotypes, as well as E6/E7 mRNA expression of high-risk HPVs (16, 18, 31, 33 and 45) in oral squamous cell carcinomas (OSCCs) from 45 Greek patients. The overall prevalence of HPV DNA positive OSCCs was 11.1% (5/45), while high-risk HPV DNA was found in 6.7% (3/45) of OSCCs. E6/E7 mRNA expression was detected in 8.9% (4/45) of the oral cavity samples. Our data indicated that HPV 16 was the commonest genotype identified in HPV-positive OSCCs by both DNA and RNA tests. This study confirms the prevalence of HPV infections among patients with OSCCs. Future analysis and followup of more OSCCs will enable us to correlate HPV detection and clinical outcome. 1. Introduction Cervical infection by one of approximately 15 high-risk HPV types is generally accepted as the necessary causative agent of cervical cancer [1, 2]. The upper aerodigestive tract, including the oral cavity, the pharynx, and the larynx, is also lined by a squamous mucous membrane and because of the morphological similarities and epitheliotropic nature of HPV, a link between head and neck squamous cell carcinoma (HNSCC) and HPV seems logical [3]. HNSCC is usually etiologically linked to tobacco and/or alcohol or other lifestyle habits, but a minority of patients develop HNSCC in the absence of exposure to these factors or any other obvious predisposing genetic defect. Several investigators have reported detection of HPV infection in healthy oral mucosa as well as in squamous cell carcinoma of the oral cavity (OSCC) and oropharynx (OPSCC) [4, 5], which are related to sexual behaviour and younger age [6]. HPV has shown to have a predilection for certain, especially nonkeratinized, anatomical sites of the oropharynx. High-risk HPV types, such as HPV 16, have been detected even in clinically normal oropharyngeal mucosa [4]. In the cervix, the persistence of HPV infection may increase the likelihood of viral integration and concomitant deregulation of viral protein expression, leading to overexpression of E6/E7 oncoproteins [7, 8]. In oral cancers the integration of HPV DNA into the host’s cell genome is probably a less common event [9]. Various HPV types have been identified in patients with oral cancer [10], but clinical and case control studies have not proved a causal relationship between the virus and oral carcinomas beyond any reasonable doubt [8, 9, 11]. HPV DNA detection alone is regarded as insufficient evidence for a causal role in oral cells