Abstract
BackgroundThe prevalence of high-risk human papillomavirus (HPV) DNA in cases of oral cavity squamous cell carcinoma (SCC) varies widely. The aim of this study is to investigate the frequency of high-risk HPV DNA in a large Brazilian cohort of patients with oral cavity SCC.MethodsBiopsy and resected frozen and formalin-fixed paraffin-embedded specimens of oral cavity SCC were available from 101 patients who were recruited at two Brazilian centres. Stringent measures with respect to case selection and prevention of sample contamination were adopted to ensure reliability of the data. Nested PCR using MY09/MY11 and GP5+/GP6+ as well as PGMY09/11 L1 consensus primers were performed to investigate the presence of HPV DNA in the tumours. HPV-positive cases were subjected to direct sequencing. Shapiro–Wilk and Student t test were used to evaluate data normality and to compare the means, respectively. Qualitative variables were analysed by logistic regression.ResultsOur results demonstrate that the frequency of high-risk HPV types in oral cavity SCC is very low and is less than 4%. All HPV-positive cases were HPV16. In addition, our results do not show a significant association between the tumour clinical features and the risk factors (tobacco, alcohol and HPV) for oral cavity SCC.ConclusionIn the current study, we observed an overlapping pattern of risk factors that are related to tumour development. This, along with a low frequency of high-risk HPV DNA, supports the findings that HPV is not involved in the genesis of oral cavity SCC in Brazilian population.
Highlights
The prevalence of high-risk human papillomavirus (HPV) DNA in cases of oral cavity squamous cell carcinoma (SCC) varies widely
human papillomavirus type 16 (HPV16)-associated carcinogenesis is mediated by expression of the viral E6 and E7 oncoproteins, which inactivate the tumour suppressor proteins p53 and retinoblastoma; this disrupts cell cycle regulatory pathways [6]
The aim of this study is to investigate the frequency of high-risk HPV in a large Brazilian cohort of patients with oral cavity SCC
Summary
The prevalence of high-risk human papillomavirus (HPV) DNA in cases of oral cavity squamous cell carcinoma (SCC) varies widely. Head and neck squamous cell carcinoma (HNSCC) is a significant cause of cancer morbidity worldwide as 650,000 new cases and 350,000 deaths occur every year [1]. HNSCC encompasses tumours of the oral cavity, oropharynx, hypopharynx and larynx, which are each associated with different risk factors and prognoses. Over the last 15 years, high-risk (HR) human papillomavirus (HPV) infection has been aetiologically linked to a subset of HNSCCs. HPV involvement in oral and oropharyngeal carcinogenesis was first proposed by Syrjanen et al in 1983 [4]. HPV16-associated carcinogenesis is mediated by expression of the viral E6 and E7 oncoproteins, which inactivate the tumour suppressor proteins p53 and retinoblastoma; this disrupts cell cycle regulatory pathways [6]. The lack of p53 mutations [7] and p16 protein accumulation [8,9,10], which occur as a result of the loss of transcriptional repression during early tumorigenesis, are considered to be hallmarks of HPV-related HNSCC [11]
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